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ESP: PubMed Auto Bibliography 03 Mar 2021 at 01:39 Created:
Evolution of Multicelluarity
Created with PubMed® Query: (evolution OR origin) AND (multicellularity OR multicellular) NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2021-03-02
CmpDate: 2021-03-02
Bacterial and Protozoan Lipoxygenases Could be Involved in Cell-to-Cell Signaling and Immune Response Suppression.
Biochemistry. Biokhimiia, 85(9):1048-1071.
Lipoxygenases are found in animals, plants, and fungi, where they are involved in a wide range of cell-to-cell signaling processes. The presence of lipoxygenases in a number of bacteria and protozoa has been also established, but their biological significance remains poorly understood. Several hypothetical functions of lipoxygenases in bacteria and protozoa have been suggested without experimental validation. The objective of our study was evaluating the functions of bacterial and protozoan lipoxygenases by evolutionary and taxonomic analysis using bioinformatics tools. Lipoxygenase sequences were identified and examined using BLAST, followed by analysis of constructed phylogenetic trees and networks. Our results support the theory on the involvement of lipoxygenases in the formation of multicellular structures by microorganisms and their possible evolutionary significance in the emergence of multicellularity. Furthermore, we observed association of lipoxygenases with the suppression of host immune response by parasitic and symbiotic bacteria including dangerous opportunistic pathogens.
Additional Links: PMID-33050851
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@article {pmid33050851,
year = {2020},
author = {Kurakin, GF and Samoukina, AM and Potapova, NA},
title = {Bacterial and Protozoan Lipoxygenases Could be Involved in Cell-to-Cell Signaling and Immune Response Suppression.},
journal = {Biochemistry. Biokhimiia},
volume = {85},
number = {9},
pages = {1048-1071},
doi = {10.1134/S0006297920090059},
pmid = {33050851},
issn = {1608-3040},
mesh = {Animals ; Bacteria/*enzymology ; *Biological Evolution ; *Cell Communication ; Humans ; Immunity/*immunology ; Lipoxygenases/*metabolism ; Protozoan Proteins/*metabolism ; },
abstract = {Lipoxygenases are found in animals, plants, and fungi, where they are involved in a wide range of cell-to-cell signaling processes. The presence of lipoxygenases in a number of bacteria and protozoa has been also established, but their biological significance remains poorly understood. Several hypothetical functions of lipoxygenases in bacteria and protozoa have been suggested without experimental validation. The objective of our study was evaluating the functions of bacterial and protozoan lipoxygenases by evolutionary and taxonomic analysis using bioinformatics tools. Lipoxygenase sequences were identified and examined using BLAST, followed by analysis of constructed phylogenetic trees and networks. Our results support the theory on the involvement of lipoxygenases in the formation of multicellular structures by microorganisms and their possible evolutionary significance in the emergence of multicellularity. Furthermore, we observed association of lipoxygenases with the suppression of host immune response by parasitic and symbiotic bacteria including dangerous opportunistic pathogens.},
}
MeSH Terms:
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Animals
Bacteria/*enzymology
*Biological Evolution
*Cell Communication
Humans
Immunity/*immunology
Lipoxygenases/*metabolism
Protozoan Proteins/*metabolism
RevDate: 2021-02-26
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition).
Autophagy [Epub ahead of print].
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.
Additional Links: PMID-33634751
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@article {pmid33634751,
year = {2021},
author = {Klionsky, DJ and Abdel-Aziz, AK and Abdelfatah, S and Abdellatif, M and Abdoli, A and Abel, S and Abeliovich, H and Abildgaard, MH and Abudu, YP and Acevedo-Arozena, A and Adamopoulos, IE and Adeli, K and Adolph, TE and Adornetto, A and Aflaki, E and Agam, G and Agarwal, A and Aggarwal, BB and Agnello, M and Agostinis, P and Agrewala, JN and Agrotis, A and Aguilar, PV and Ahmad, ST and Ahmed, ZM and Ahumada-Castro, U and Aits, S and Aizawa, S and Akkoc, Y and Akoumianaki, T and Akpinar, HA and Al-Abd, AM and Al-Akra, L and Al-Gharaibeh, A and Alaoui-Jamali, MA and Alberti, S and Alcocer-Gómez, E and Alessandri, C and Ali, M and Alim Al-Bari, MA and Aliwaini, S and Alizadeh, J and Almacellas, E and Almasan, A and Alonso, A and Alonso, GD and Altan-Bonnet, N and Altieri, DC and Álvarez, ÉMC and Alves, S and Alves da Costa, C and Alzaharna, MM and Amadio, M and Amantini, C and Amaral, C and Ambrosio, S and Amer, AO and Ammanathan, V and An, Z and Andersen, SU and Andrabi, SA and Andrade-Silva, M and Andres, AM and Angelini, S and Ann, D and Anozie, UC and Ansari, MY and Antas, P and Antebi, A and Antón, Z and Anwar, T and Apetoh, L and Apostolova, N and Araki, T and Araki, Y and Arasaki, K and Araújo, WL and Araya, J and Arden, C and Arévalo, MA and Arguelles, S and Arias, E and Arikkath, J and Arimoto, H and Ariosa, AR and Armstrong-James, D and Arnauné-Pelloquin, L and Aroca, A and Arroyo, DS and Arsov, I and Artero, R and Asaro, DML and Aschner, M and Ashrafizadeh, M and Ashur-Fabian, O and Atanasov, AG and Au, AK and Auberger, P and Auner, HW and Aurelian, L and Autelli, R and Avagliano, L and Ávalos, Y and Aveic, S and Aveleira, CA and Avin-Wittenberg, T and Aydin, Y and Ayton, S and Ayyadevara, S and Azzopardi, M and Baba, M and Backer, JM and Backues, SK and Bae, DH and Bae, ON and Bae, SH and Baehrecke, EH and Baek, A and Baek, SH and Baek, SH and Bagetta, G and Bagniewska-Zadworna, A and Bai, H and Bai, J and Bai, X and Bai, Y and Bairagi, N and 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and Bergami, M and Bergmann, A and Berliocchi, L and Berlioz-Torrent, C and Bernard, A and Berthoux, L and Besirli, CG and Besteiro, S and Betin, VM and Beyaert, R and Bezbradica, JS and Bhaskar, K and Bhatia-Kissova, I and Bhattacharya, R and Bhattacharya, S and Bhattacharyya, S and Bhuiyan, MS and Bhutia, SK and Bi, L and Bi, X and Biden, TJ and Bijian, K and Billes, VA and Binart, N and Bincoletto, C and Birgisdottir, AB and Bjorkoy, G and Blanco, G and Blas-Garcia, A and Blasiak, J and Blomgran, R and Blomgren, K and Blum, JS and Boada-Romero, E and Boban, M and Boesze-Battaglia, K and Boeuf, P and Boland, B and Bomont, P and Bonaldo, P and Bonam, SR and Bonfili, L and Bonifacino, JS and Boone, BA and Bootman, MD and Bordi, M and Borner, C and Bornhauser, BC and Borthakur, G and Bosch, J and Bose, S and Botana, LM and Botas, J and Boulanger, CM and Boulton, ME and Bourdenx, M and Bourgeois, B and Bourke, NM and Bousquet, G and Boya, P and Bozhkov, PV and Bozi, LHM and Bozkurt, TO and Brackney, DE and Brandts, CH and Braun, RJ and Braus, GH and Bravo-Sagua, R and Bravo-San Pedro, JM and Brest, P and Bringer, MA and Briones-Herrera, A and Broaddus, VC and Brodersen, P and Brodsky, JL and Brody, SL and Bronson, PG and Bronstein, JM and Brown, CN and Brown, RE and Brum, PC and Brumell, JH and Brunetti-Pierri, N and Bruno, D and Bryson-Richardson, RJ and Bucci, C and Buchrieser, C and Bueno, M and Buitrago-Molina, LE and Buraschi, S and Buch, S and Buchan, JR and Buckingham, EM and Budak, H and Budini, M and Bultynck, G and Burada, F and Burgoyne, JR and Burón, MI and Bustos, V and Büttner, S and Butturini, E and Byrd, A and Cabas, I and Cabrera-Benitez, S and Cadwell, K and Cai, J and Cai, L and Cai, Q and Cairó, M and Calbet, JA and Caldwell, GA and Caldwell, KA and Call, JA and Calvani, R and Calvo, AC and Calvo-Rubio Barrera, M and Camara, NO and Camonis, JH and Camougrand, N and Campanella, M and Campbell, EM and Campbell-Valois, FX and Campello, S and Campesi, I and Campos, JC and Camuzard, O and Cancino, J and Candido de Almeida, D and Canesi, L and Caniggia, I and Canonico, B and Cantí, C and Cao, B and Caraglia, M and Caramés, B and Carchman, EH and Cardenal-Muñoz, E and Cardenas, C and Cardenas, L and Cardoso, SM and Carew, JS and Carle, GF and Carleton, G and Carloni, S and Carmona-Gutierrez, D and Carneiro, LA and Carnevali, O and Carosi, JM and Carra, S and Carrier, A and Carrier, L and Carroll, B and Carter, AB and Carvalho, AN and Casanova, M and Casas, C and Casas, J and Cassioli, C and Castillo, EF and Castillo, K and Castillo-Lluva, S and Castoldi, F and Castori, M and Castro, AF and Castro-Caldas, M and Castro-Hernandez, J and Castro-Obregon, S and Catz, SD and Cavadas, C and Cavaliere, F and Cavallini, G and Cavinato, M and Cayuela, ML and Cebollada Rica, P and Cecarini, V and Cecconi, F and Cechowska-Pasko, M and Cenci, S and Ceperuelo-Mallafré, V and Cerqueira, JJ and Cerutti, JM and Cervia, D and Cetintas, VB and Cetrullo, S and Chae, HJ and Chagin, AS and Chai, CY and Chakrabarti, G and Chakrabarti, O and Chakraborty, T and Chakraborty, T and Chami, M and Chamilos, G and Chan, DW and Chan, EYW and Chan, ED and Chan, HYE and Chan, HH and Chan, H and Chan, MTV and Chan, YS and Chandra, PK and Chang, CP and Chang, C and Chang, HC and Chang, K and Chao, J and Chapman, T and Charlet-Berguerand, N and Chatterjee, S and Chaube, SK and Chaudhary, A and Chauhan, S and Chaum, E and Checler, F and Cheetham, ME and Chen, CS and Chen, GC and Chen, JF and Chen, LL and Chen, L and Chen, L and Chen, M and Chen, MK and Chen, N and Chen, Q and Chen, RH and Chen, S and Chen, W and Chen, W and Chen, XM and Chen, XW and Chen, X and Chen, Y and Chen, YG and Chen, Y and Chen, Y and Chen, YJ and Chen, YQ and Chen, ZS and Chen, Z and Chen, ZH and Chen, ZJ and Chen, Z and Cheng, H and Cheng, J and Cheng, SY and Cheng, W and Cheng, X and Cheng, XT and Cheng, Y and Cheng, Z and Chen, Z and Cheong, H and Cheong, JK and Chernyak, BV and Cherry, S and Cheung, CFR and Cheung, CHA and Cheung, KH and Chevet, E and Chi, RJ and Chiang, AKS and Chiaradonna, F and Chiarelli, R and Chiariello, M and Chica, N and Chiocca, S and Chiong, M and Chiou, SH and Chiramel, AI and Chiurchiù, V and Cho, DH and Choe, SK and Choi, AMK and Choi, ME and Choudhury, KR and Chow, NS and Chu, CT and Chua, JP and Chua, JJE and Chung, H and Chung, KP and Chung, S and Chung, SH and Chung, YL and Cianfanelli, V and Ciechomska, IA and Cifuentes, M and Cinque, L and Cirak, S and Cirone, M and Clague, MJ and Clarke, R and Clementi, E and Coccia, EM and Codogno, P and Cohen, E and Cohen, MM and Colasanti, T and Colasuonno, F and Colbert, RA and Colell, A and Čolić, M and Coll, NS and Collins, MO and Colombo, MI and Colón-Ramos, DA and Combaret, L and Comincini, S and Cominetti, MR and Consiglio, A and Conte, A and Conti, F and Contu, VR and Cookson, MR and Coombs, KM and Coppens, I and Corasaniti, MT and Corkery, DP and Cordes, N and Cortese, K and Costa, MDC and Costantino, S and Costelli, P and Coto-Montes, A and Crack, PJ and Crespo, JL and Criollo, A and Crippa, V and Cristofani, R and Csizmadia, T and Cuadrado, A and Cui, B and Cui, J and Cui, Y and Cui, Y and Culetto, E and Cumino, AC and Cybulsky, AV and Czaja, MJ and Czuczwar, SJ and D'Adamo, S and D'Amelio, M and D'Arcangelo, D and D'Lugos, AC and D'Orazi, G and da Silva, JA and Dafsari, HS and Dagda, RK and Dagdas, Y and Daglia, M and Dai, X and Dai, Y and Dai, Y and Dal Col, J and Dalhaimer, P and Dalla Valle, L and Dallenga, T and Dalmasso, G and Damme, M and Dando, I and Dantuma, NP and Darling, AL and Das, H and Dasarathy, S and Dasari, SK and Dash, S and Daumke, O and Dauphinee, AN and Davies, JS and Dávila, VA and Davis, RJ and Davis, T and Dayalan Naidu, S and De Amicis, F and De Bosscher, K and De Felice, F and De Franceschi, L and De Leonibus, C and de Mattos Barbosa, MG and De Meyer, GRY and De Milito, A and De Nunzio, C and De Palma, C and De Santi, M and De Virgilio, C and De Zio, D and Debnath, J and DeBosch, BJ and Decuypere, JP and Deehan, MA and Deflorian, G and DeGregori, J and Dehay, B and Del Rio, G and Delaney, JR and Delbridge, LMD and Delorme-Axford, E and Delpino, MV and Demarchi, F and Dembitz, V and Demers, ND and Deng, H and Deng, Z and Dengjel, J and Dent, P and Denton, D and DePamphilis, ML and Der, CJ and Deretic, V and Descoteaux, A and Devis, L and Devkota, S and Devuyst, O and Dewson, G and Dharmasivam, M and Dhiman, R and di Bernardo, D and Di Cristina, M and Di Domenico, F and Di Fazio, P and Di Fonzo, A and Di Guardo, G and Di Guglielmo, GM and Di Leo, L and Di Malta, C and Di Nardo, A and Di Rienzo, M and Di Sano, F and Diallinas, G and Diao, J and Diaz-Araya, G and Díaz-Laviada, I and Dickinson, JM and Diederich, M and Dieudé, M and Dikic, I and Ding, S and Ding, WX and Dini, L and Dinić, J and Dinic, M and Dinkova-Kostova, AT and Dionne, MS and Distler, JHW and Diwan, A and Dixon, IMC and Djavaheri-Mergny, M and 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and Hwang, HY and Hwang, S and Ieni, A and Ikeda, F and Imagawa, Y and Imai, Y and Imbriano, C and Imoto, M and Inman, DM and Inoki, K and Iovanna, J and Iozzo, RV and Ippolito, G and Irazoqui, JE and Iribarren, P and Ishaq, M and Ishikawa, M and Ishimwe, N and Isidoro, C and Ismail, N and Issazadeh-Navikas, S and Itakura, E and Ito, D and Ivankovic, D and Ivanova, S and Iyer, AKV and Izquierdo, JM and Izumi, M and Jäättelä, M and Jabir, MS and Jackson, WT and Jacobo-Herrera, N and Jacomin, AC and Jacquin, E and Jadiya, P and Jaeschke, H and Jagannath, C and Jakobi, AJ and Jakobsson, J and Janji, B and Jansen-Dürr, P and Jansson, PJ and Jantsch, J and Januszewski, S and Jassey, A and Jean, S and Jeltsch-David, H and Jendelova, P and Jenny, A and Jensen, TE and Jessen, N and Jewell, JL and Ji, J and Jia, L and Jia, R and Jiang, L and Jiang, Q and Jiang, R and Jiang, T and Jiang, X and Jiang, Y and Jimenez-Sanchez, M and Jin, EJ and Jin, F and Jin, H and Jin, L and Jin, L and Jin, M and 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Kemper, JK and Kenific, CM and Kepp, O and Kermorgant, S and Kern, A and Ketteler, R and Keulers, TG and Khalfin, B and Khalil, H and Khambu, B and Khan, SY and Khandelwal, VKM and Khandia, R and Kho, W and Khobrekar, NV and Khuansuwan, S and Khundadze, M and Killackey, SA and Kim, D and Kim, DR and Kim, DH and Kim, DE and Kim, EY and Kim, EK and Kim, HR and Kim, HS and Hyung-Ryong Kim, and Kim, JH and Kim, JK and Kim, JH and Kim, J and Kim, JH and Kim, KI and Kim, PK and Kim, SJ and Kimball, SR and Kimchi, A and Kimmelman, AC and Kimura, T and King, MA and Kinghorn, KJ and Kinsey, CG and Kirkin, V and Kirshenbaum, LA and Kiselev, SL and Kishi, S and Kitamoto, K and Kitaoka, Y and Kitazato, K and Kitsis, RN and Kittler, JT and Kjaerulff, O and Klein, PS and Klopstock, T and Klucken, J and Knævelsrud, H and Knorr, RL and Ko, BCB and Ko, F and Ko, JL and Kobayashi, H and Kobayashi, S and Koch, I and Koch, JC and Koenig, U and Kögel, D and Koh, YH and Koike, M and Kohlwein, SD and Kocaturk, NM and Komatsu, M and König, J and Kono, T and Kopp, BT and Korcsmaros, T and Korkmaz, G and Korolchuk, VI and Korsnes, MS and Koskela, A and Kota, J and Kotake, Y and Kotler, ML and Kou, Y and Koukourakis, MI and Koustas, E and Kovacs, AL and Kovács, T and Koya, D and Kozako, T and Kraft, C and Krainc, D and Krämer, H and Krasnodembskaya, AD and Kretz-Remy, C and Kroemer, G and Ktistakis, NT and Kuchitsu, K and Kuenen, S and Kuerschner, L and Kukar, T and Kumar, A and Kumar, A and Kumar, D and Kumar, D and Kumar, S and Kume, S and Kumsta, C and Kundu, CN and Kundu, M and Kunnumakkara, AB and Kurgan, L and Kutateladze, TG and Kutlu, O and Kwak, S and Kwon, HJ and Kwon, TK and Kwon, YT and Kyrmizi, I and La Spada, A and Labonté, P and Ladoire, S and Laface, I and Lafont, F and Lagace, DC and Lahiri, V and Lai, Z and Laird, AS and Lakkaraju, A and Lamark, T and Lan, SH and Landajuela, A and Lane, DJR and Lane, JD and Lang, CH and Lange, C and Langel, Ü and Langer, R and Lapaquette, P and Laporte, J and LaRusso, NF and Lastres-Becker, I and Lau, WCY and Laurie, GW and Lavandero, S and Law, BYK and Law, HK and Layfield, R and Le, W and Le Stunff, H and Leary, AY and Lebrun, JJ and Leck, LYW and Leduc-Gaudet, JP and Lee, C and Lee, CP and Lee, DH and Lee, EB and Lee, EF and Lee, GM and Lee, HJ and Lee, HK and Lee, JM and Lee, JS and Lee, JA and Lee, JY and Lee, JH and Lee, M and Lee, MG and Lee, MJ and Lee, MS and Lee, SY and Lee, SJ and Lee, SY and Lee, SB and Lee, WH and Lee, YR and Lee, YH and Lee, Y and Lefebvre, C and Legouis, R and Lei, YL and Lei, Y and Leikin, S and Leitinger, G and Lemus, L and Leng, S and Lenoir, O and Lenz, G and Lenz, HJ and Lenzi, P and León, Y and Leopoldino, AM and Leschczyk, C and Leskelä, S and Letellier, E and Leung, CT and Leung, PS and Leventhal, JS and Levine, B and Lewis, PA and Ley, K and Li, B and Li, DQ and Li, J and Li, J and Li, J and Li, K and Li, L and Li, M and Li, M and Li, M and Li, M and Li, M and Li, PL and Li, MQ and Li, Q and Li, S and Li, T and Li, W and Li, W and Li, X and Li, YP and Li, Y and Li, Z and Li, Z and Li, Z and Lian, J and Liang, C and Liang, Q and Liang, W and Liang, Y and Liang, Y and Liao, G and Liao, L and Liao, M and Liao, YF and Librizzi, M and Lie, PPY and Lilly, MA and Lim, HJ and Lima, TRR and Limana, F and Lin, C and Lin, CW and Lin, DS and Lin, FC and Lin, JD and Lin, KM and Lin, KH and Lin, LT and Lin, PH and Lin, Q and Lin, S and Lin, SJ and Lin, W and Lin, X and Lin, YX and Lin, YS and Linden, R and Lindner, P and Ling, SC and Lingor, P and Linnemann, AK and Liou, YC and Lipinski, MM and Lipovšek, S and Lira, VA and Lisiak, N and Liton, PB and Liu, C and Liu, CH and Liu, CF and Liu, CH and Liu, F and Liu, H and Liu, HS and Liu, HF and Liu, H and Liu, J and Liu, J and Liu, J and Liu, L and Liu, L and Liu, M and Liu, Q and Liu, W and Liu, W and Liu, XH and Liu, X and Liu, X and Liu, X and Liu, X and Liu, Y and Liu, Y and Liu, Y and Liu, Y and Liu, Y and 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MacKeigan, JP and Macleod, KF and Maday, S and Madeo, F and Madesh, M and Madl, T and Madrigal-Matute, J and Maeda, A and Maejima, Y and Magarinos, M and Mahavadi, P and Maiani, E and Maiese, K and Maiti, P and Maiuri, MC and Majello, B and Major, MB and Makareeva, E and Malik, F and Mallilankaraman, K and Malorni, W and Maloyan, A and Mammadova, N and Man, GCW and Manai, F and Mancias, JD and Mandelkow, EM and Mandell, MA and Manfredi, AA and Manjili, MH and Manjithaya, R and Manque, P and Manshian, BB and Manzano, R and Manzoni, C and Mao, K and Marchese, C and Marchetti, S and Marconi, AM and Marcucci, F and Mardente, S and Mareninova, OA and Margeta, M and Mari, M and Marinelli, S and Marinelli, O and Mariño, G and Mariotto, S and Marshall, RS and Marten, MR and Martens, S and Martin, APJ and Martin, KR and Martin, S and Martin, S and Martín-Segura, A and Martín-Acebes, MA and Martin-Burriel, I and Martin-Rincon, M and Martin-Sanz, P and Martina, JA and Martinet, W and Martinez, A 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Ojha, R and Okamoto, K and Okazawa, H and Oku, M and Oliván, S and Oliveira, JMA and Ollmann, M and Olzmann, JA and Omari, S and Omary, MB and Önal, G and Ondrej, M and Ong, SB and Ong, SG and Onnis, A and Orellana, JA and Orellana-Muñoz, S and Ortega-Villaizan, MDM and Ortiz-Gonzalez, XR and Ortona, E and Osiewacz, HD and Osman, AK and Osta, R and Otegui, MS and Otsu, K and Ott, C and Ottobrini, L and Ou, JJ and Outeiro, TF and Oynebraten, I and Ozturk, M and Pagès, G and Pahari, S and Pajares, M and Pajvani, UB and Pal, R and Paladino, S and Pallet, N and Palmieri, M and Palmisano, G and Palumbo, C and Pampaloni, F and Pan, L and Pan, Q and Pan, W and Pan, X and Panasyuk, G and Pandey, R and Pandey, UB and Pandya, V and Paneni, F and Pang, SY and Panzarini, E and Papademetrio, DL and Papaleo, E and Papinski, D and Papp, D and Park, EC and Park, HT and Park, JM and Park, JI and Park, JT and Park, J and Park, SC and Park, SY and Parola, AH and Parys, JB and Pasquier, A and Pasquier, B 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Singh, S and Singh, SP and Sinha, D and Sinha, RA and Sinha, S and Sirko, A and Sirohi, K and Sivridis, EL and Skendros, P and Skirycz, A and Slaninová, I and Smaili, SS and Smertenko, A and Smith, MD and Soenen, SJ and Sohn, EJ and Sok, SPM and Solaini, G and Soldati, T and Soleimanpour, SA and Soler, RM and Solovchenko, A and Somarelli, JA and Sonawane, A and Song, F and Song, HK and Song, JX and Song, K and Song, Z and Soria, LR and Sorice, M and Soukas, AA and Soukup, SF and Sousa, D and Sousa, N and Spagnuolo, PA and Spector, SA and Srinivas Bharath, MM and St Clair, D and Stagni, V and Staiano, L and Stalnecker, CA and Stankov, MV and Stathopulos, PB and Stefan, K and Stefan, SM and Stefanis, L and Steffan, JS and Steinkasserer, A and Stenmark, H and Sterneckert, J and Stevens, C and Stoka, V and Storch, S and Stork, B and Strappazzon, F and Strohecker, AM and Stupack, DG and Su, H and Su, LY and Su, L and Suarez-Fontes, AM and Subauste, CS and Subbian, S and Subirada, PV and Sudhandiran, G and Sue, CM and Sui, X and Summers, C and Sun, G and Sun, J and Sun, K and Sun, MX and Sun, Q and Sun, Y and Sun, Z and Sunahara, KKS and Sundberg, E and Susztak, K and Sutovsky, P and Suzuki, H and Sweeney, G and Symons, JD and Sze, SCW and Szewczyk, NJ and Tabęcka-Łonczynska, A and Tabolacci, C and Tacke, F and Taegtmeyer, H and Tafani, M and Tagaya, M and Tai, H and Tait, SWG and Takahashi, Y and Takats, S and Talwar, P and Tam, C and Tam, SY and Tampellini, D and Tamura, A and Tan, CT and Tan, EK and Tan, YQ and Tanaka, M and Tanaka, M and Tang, D and Tang, J and Tang, TS and Tanida, I and Tao, Z and Taouis, M and Tatenhorst, L and Tavernarakis, N and Taylor, A and Taylor, GA and Taylor, JM and Tchetina, E and Tee, AR and Tegeder, I and Teis, D and Teixeira, N and Teixeira-Clerc, F and Tekirdag, KA and Tencomnao, T and Tenreiro, S and Tepikin, AV and Testillano, PS and Tettamanti, G and Tharaux, PL and Thedieck, K and Thekkinghat, AA and Thellung, S and Thinwa, JW and Thirumalaikumar, VP and Thomas, SM and Thomes, PG and Thorburn, A and Thukral, L and Thum, T and Thumm, M and Tian, L and Tichy, A and Till, A and Timmerman, V and Titorenko, VI and Todi, SV and Todorova, K and Toivonen, JM and Tomaipitinca, L and Tomar, D and Tomas-Zapico, C and Tomić, S and Tong, BC and Tong, C and Tong, X and Tooze, SA and Torgersen, ML and Torii, S and Torres-López, L and Torriglia, A and Towers, CG and Towns, R and Toyokuni, S and Trajkovic, V and Tramontano, D and Tran, QG and Travassos, LH and Trelford, CB and Tremel, S and Trougakos, IP and Tsao, BP and Tschan, MP and Tse, HF and Tse, TF and Tsugawa, H and Tsvetkov, AS and Tumbarello, DA and Tumtas, Y and Tuñón, MJ and Turcotte, S and Turk, B and Turk, V and Turner, BJ and Tuxworth, RI and Tyler, JK and Tyutereva, EV and Uchiyama, Y and Ugun-Klusek, A and Uhlig, HH and Ułamek-Kozioł, M and Ulasov, IV and Umekawa, M and Ungermann, C and Unno, R and Urbe, S and Uribe-Carretero, E and Üstün, S and Uversky, VN and Vaccari, T and Vaccaro, MI and Vahsen, BF and Vakifahmetoglu-Norberg, H and Valdor, R and Valente, MJ and Valko, A and Vallee, RB and Valverde, AM and Van den Berghe, G and van der Veen, S and Van Kaer, L and van Loosdregt, J and van Wijk, SJL and Vandenberghe, W and Vanhorebeek, I and Vannier-Santos, MA and Vannini, N and Vanrell, MC and Vantaggiato, C and Varano, G and Varela-Nieto, I and Varga, M and Vasconcelos, MH and Vats, S and Vavvas, DG and Vega-Naredo, I and Vega-Rubin-de-Celis, S and Velasco, G and Velázquez, AP and Vellai, T and Vellenga, E and Velotti, F and Verdier, M and Verginis, P and Vergne, I and Verkade, P and Verma, M and Verstreken, P and Vervliet, T and Vervoorts, J and Vessoni, AT and Victor, VM and Vidal, M and Vidoni, C and Vieira, OV and Vierstra, RD and Viganó, S and Vihinen, H and Vijayan, V and Vila, M and Vilar, M and Villalba, JM and Villalobo, A and Villarejo-Zori, B and Villarroya, F and Villarroya, J and Vincent, O and Vindis, C and Viret, C and Viscomi, MT and Visnjic, D and Vitale, I and Vocadlo, DJ and Voitsekhovskaja, OV and Volonté, C and Volta, M and Vomero, M and Von Haefen, C and Vooijs, MA and Voos, W and Vucicevic, L and Wade-Martins, R and Waguri, S and Waite, KA and Wakatsuki, S and Walker, DW and Walker, MJ and Walker, SA and Walter, J and Wandosell, FG and Wang, B and Wang, CY and Wang, C and Wang, C and Wang, C and Wang, CY and Wang, D and Wang, F and Wang, F and Wang, F and Wang, G and Wang, H and Wang, H and Wang, H and Wang, HG and Wang, J and Wang, J and Wang, J and Wang, J and Wang, K and Wang, L and Wang, L and Wang, MH and Wang, M and Wang, N and Wang, P and Wang, P and Wang, P and Wang, P and Wang, QJ and Wang, Q and Wang, QK and Wang, QA and Wang, WT and Wang, W and Wang, X and Wang, X and Wang, Y and Wang, Y and Wang, Y and Wang, YY and Wang, Y and Wang, Y and Wang, Y and Wang, Y and Wang, Z and Wang, Z and Wang, Z and Warnes, G and Warnsmann, V and Watada, H and Watanabe, E and Watchon, M and Wawrzyńska, A and Weaver, TE and Wegrzyn, G and Wehman, AM and Wei, H and Wei, L and Wei, T and Wei, Y and Weiergräber, OH and Weihl, CC and Weindl, G and Weiskirchen, R and Wells, A and Wen, RH and Wen, X and Werner, A and Weykopf, B and Wheatley, SP and Whitton, JL and Whitworth, AJ and Wiktorska, K and Wildenberg, ME and Wileman, T and Wilkinson, S and Willbold, D and Williams, B and Williams, RSB and Williams, RL and Williamson, PR and Wilson, RA and Winner, B and Winsor, NJ and Witkin, SS and Wodrich, H and Woehlbier, U and Wollert, T and Wong, E and Wong, JH and Wong, RW and Wong, VKW and Wong, WW and Wu, AG and Wu, C and Wu, J and Wu, J and Wu, KK and Wu, M and Wu, SY and Wu, S and Wu, SY and Wu, S and Wu, WKK and Wu, X and Wu, X and Wu, YW and Wu, Y and Xavier, RJ and Xia, H and Xia, L and Xia, Z and Xiang, G and Xiang, J and Xiang, M and Xiang, W and Xiao, B and Xiao, G and Xiao, H and Xiao, HT and Xiao, J and Xiao, L and Xiao, S and Xiao, Y and Xie, B and Xie, CM and Xie, M and Xie, Y and Xie, Z and Xie, Z and Xilouri, M and Xu, C and Xu, E and Xu, H and Xu, J and Xu, J and Xu, L and Xu, WW and Xu, X and Xue, Y and Yakhine-Diop, SMS and Yamaguchi, M and Yamaguchi, O and Yamamoto, A and Yamashina, S and Yan, S and Yan, SJ and Yan, Z and Yanagi, Y and Yang, C and Yang, DS and Yang, H and Yang, HT and Yang, H and Yang, JM and Yang, J and Yang, J and Yang, L and Yang, L and Yang, M and Yang, PM and Yang, Q and Yang, S and Yang, S and Yang, SF and Yang, W and Yang, WY and Yang, X and Yang, X and Yang, Y and Yang, Y and Yao, H and Yao, S and Yao, X and Yao, YG and Yao, YM and Yasui, T and Yazdankhah, M and Yen, PM and Yi, C and Yin, XM and Yin, Y and Yin, Z and Yin, Z and Ying, M and Ying, Z and Yip, CK and Yiu, SPT and Yoo, YH and Yoshida, K and Yoshii, SR and Yoshimori, T and Yousefi, B and Yu, B and Yu, H and Yu, J and Yu, J and Yu, L and Yu, ML and Yu, SW and Yu, VC and Yu, WH and Yu, Z and Yu, Z and Yuan, J and Yuan, LQ and Yuan, S and Yuan, SF and Yuan, Y and Yuan, Z and Yue, J and Yue, Z and Yun, J and Yung, RL and Zacks, DN and Zaffagnini, G and Zambelli, VO and Zanella, I and Zang, QS and Zanivan, S and Zappavigna, S and Zaragoza, P and Zarbalis, KS and Zarebkohan, A and Zarrouk, A and Zeitlin, SO and Zeng, J and Zeng, JD and Žerovnik, E and Zhan, L and Zhang, B and Zhang, DD and Zhang, H and Zhang, H and Zhang, H and Zhang, H and Zhang, H and Zhang, H and Zhang, H and Zhang, HL and Zhang, J and Zhang, J and Zhang, JP and Zhang, KYB and Zhang, LW and Zhang, L and Zhang, L and Zhang, L and Zhang, L and Zhang, M and Zhang, P and Zhang, S and Zhang, W and Zhang, X and Zhang, XW and Zhang, X and Zhang, X and Zhang, X and Zhang, X and Zhang, XD and Zhang, Y and Zhang, Y and Zhang, Y and Zhang, YD and Zhang, Y and Zhang, YY and Zhang, Y and Zhang, Z and Zhang, Z and Zhang, Z and Zhang, Z and Zhang, Z and Zhang, Z and Zhao, H and Zhao, L and Zhao, S and Zhao, T and Zhao, XF and Zhao, Y and Zhao, Y and Zhao, Y and Zhao, Y and Zheng, G and Zheng, K and Zheng, L and Zheng, S and Zheng, XL and Zheng, Y and Zheng, ZG and Zhivotovsky, B and Zhong, Q and Zhou, A and Zhou, B and Zhou, C and Zhou, G and Zhou, H and Zhou, H and Zhou, H and Zhou, J and Zhou, J and Zhou, J and Zhou, J and Zhou, K and Zhou, R and Zhou, XJ and Zhou, Y and Zhou, Y and Zhou, Y and Zhou, ZY and Zhou, Z and Zhu, B and Zhu, C and Zhu, GQ and Zhu, H and Zhu, H and Zhu, H and Zhu, WG and Zhu, Y and Zhu, Y and Zhuang, H and Zhuang, X and Zientara-Rytter, K and Zimmermann, CM and Ziviani, E and Zoladek, T and Zong, WX and Zorov, DB and Zorzano, A and Zou, W and Zou, Z and Zou, Z and Zuryn, S and Zwerschke, W and Brand-Saberi, B and Dong, XC and Kenchappa, CS and Li, Z and Lin, Y and Oshima, S and Rong, Y and Sluimer, JC and Stallings, CL and Tong, CK},
title = {Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition).},
journal = {Autophagy},
volume = {},
number = {},
pages = {1-382},
doi = {10.1080/15548627.2020.1797280},
pmid = {33634751},
issn = {1554-8635},
abstract = {In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.},
}
RevDate: 2021-02-24
Evolution and diversity of semaphorins and plexins in choanoflagellates.
Genome biology and evolution pii:6149127 [Epub ahead of print].
Semaphorins and plexins are cell surface ligand/receptor proteins that affect cytoskeletal dynamics in metazoan cells. Interestingly, they are also present in Choanoflagellata, a class of unicellular heterotrophic flagellates that forms the phylogenetic sister group to Metazoa. Several members of choanoflagellates are capable of forming transient colonies, while others reside solitary inside exoskeletons; their molecular diversity is only beginning to emerge. Here, we surveyed genomics data from 22 choanoflagellate species and detected semaphorin/plexin pairs in 16 species. Choanoflagellate semaphorins (Sema-FN1) contain several domain features distinct from metazoan semaphorins, including an N-terminal Reeler domain that may facilitate dimer stabilization, an array of fibronectin type III domains, a variable serine/threonine-rich domain that is a potential site for O-linked glycosylation, and a SEA domain that can undergo autoproteolysis. In contrast, choanoflagellate plexins (Plexin-1) harbor a largely identical domain arrangement as metazoan plexins. Both Sema-FN1 and Plexin-1 also contain a short homologous motif near the C-terminus, likely associated with a shared function. Three-dimensional molecular models revealed a highly conserved structural architecture between choanoflagellate Plexin-1 and metazoan plexins, including similar conformational changes in a segment that can lead to activation of the intracellular Ras-GAP domain. The absence of semaphorins and plexins in several choanoflagellate species did not appear to correlate with unicellular vs. colonial lifestyle or ecological factors such as fresh vs. salt water environment. Together, our findings support a conserved mechanism of semaphorin/plexin proteins in regulating cytoskeletal dynamics in unicellular and multicellular organisms.
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@article {pmid33624753,
year = {2021},
author = {Alves, CJ and Ladeira, J and Hannah, T and Dias, RJP and Capriles, PVZ and Yotoko, K and Zou, H and Friedel, RH},
title = {Evolution and diversity of semaphorins and plexins in choanoflagellates.},
journal = {Genome biology and evolution},
volume = {},
number = {},
pages = {},
doi = {10.1093/gbe/evab035},
pmid = {33624753},
issn = {1759-6653},
abstract = {Semaphorins and plexins are cell surface ligand/receptor proteins that affect cytoskeletal dynamics in metazoan cells. Interestingly, they are also present in Choanoflagellata, a class of unicellular heterotrophic flagellates that forms the phylogenetic sister group to Metazoa. Several members of choanoflagellates are capable of forming transient colonies, while others reside solitary inside exoskeletons; their molecular diversity is only beginning to emerge. Here, we surveyed genomics data from 22 choanoflagellate species and detected semaphorin/plexin pairs in 16 species. Choanoflagellate semaphorins (Sema-FN1) contain several domain features distinct from metazoan semaphorins, including an N-terminal Reeler domain that may facilitate dimer stabilization, an array of fibronectin type III domains, a variable serine/threonine-rich domain that is a potential site for O-linked glycosylation, and a SEA domain that can undergo autoproteolysis. In contrast, choanoflagellate plexins (Plexin-1) harbor a largely identical domain arrangement as metazoan plexins. Both Sema-FN1 and Plexin-1 also contain a short homologous motif near the C-terminus, likely associated with a shared function. Three-dimensional molecular models revealed a highly conserved structural architecture between choanoflagellate Plexin-1 and metazoan plexins, including similar conformational changes in a segment that can lead to activation of the intracellular Ras-GAP domain. The absence of semaphorins and plexins in several choanoflagellate species did not appear to correlate with unicellular vs. colonial lifestyle or ecological factors such as fresh vs. salt water environment. Together, our findings support a conserved mechanism of semaphorin/plexin proteins in regulating cytoskeletal dynamics in unicellular and multicellular organisms.},
}
RevDate: 2021-02-24
Developmental processes in Ediacara macrofossils.
Proceedings. Biological sciences, 288(1945):20203055.
The Ediacara Biota preserves the oldest fossil evidence of abundant, complex metazoans. Despite their significance, assigning individual taxa to specific phylogenetic groups has proved problematic. To better understand these forms, we identify developmentally controlled characters in representative taxa from the Ediacaran White Sea assemblage and compare them with the regulatory tools underlying similar traits in modern organisms. This analysis demonstrates that the genetic pathways for multicellularity, axial polarity, musculature, and a nervous system were likely present in some of these early animals. Equally meaningful is the absence of evidence for major differentiation of macroscopic body units, including distinct organs, localized sensory machinery or appendages. Together these traits help to better constrain the phylogenetic position of several key Ediacara taxa and inform our views of early metazoan evolution. An apparent lack of heads with concentrated sensory machinery or ventral nerve cords in such taxa supports the hypothesis that these evolved independently in disparate bilaterian clades.
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@article {pmid33622124,
year = {2021},
author = {Evans, SD and Droser, ML and Erwin, DH},
title = {Developmental processes in Ediacara macrofossils.},
journal = {Proceedings. Biological sciences},
volume = {288},
number = {1945},
pages = {20203055},
doi = {10.1098/rspb.2020.3055},
pmid = {33622124},
issn = {1471-2954},
abstract = {The Ediacara Biota preserves the oldest fossil evidence of abundant, complex metazoans. Despite their significance, assigning individual taxa to specific phylogenetic groups has proved problematic. To better understand these forms, we identify developmentally controlled characters in representative taxa from the Ediacaran White Sea assemblage and compare them with the regulatory tools underlying similar traits in modern organisms. This analysis demonstrates that the genetic pathways for multicellularity, axial polarity, musculature, and a nervous system were likely present in some of these early animals. Equally meaningful is the absence of evidence for major differentiation of macroscopic body units, including distinct organs, localized sensory machinery or appendages. Together these traits help to better constrain the phylogenetic position of several key Ediacara taxa and inform our views of early metazoan evolution. An apparent lack of heads with concentrated sensory machinery or ventral nerve cords in such taxa supports the hypothesis that these evolved independently in disparate bilaterian clades.},
}
RevDate: 2021-02-24
The origin of animals: an ancestral reconstruction of the unicellular-to-multicellular transition.
Open biology, 11(2):200359.
How animals evolved from a single-celled ancestor, transitioning from a unicellular lifestyle to a coordinated multicellular entity, remains a fascinating question. Key events in this transition involved the emergence of processes related to cell adhesion, cell-cell communication and gene regulation. To understand how these capacities evolved, we need to reconstruct the features of both the last common multicellular ancestor of animals and the last unicellular ancestor of animals. In this review, we summarize recent advances in the characterization of these ancestors, inferred by comparative genomic analyses between the earliest branching animals and those radiating later, and between animals and their closest unicellular relatives. We also provide an updated hypothesis regarding the transition to animal multicellularity, which was likely gradual and involved the use of gene regulatory mechanisms in the emergence of early developmental and morphogenetic plans. Finally, we discuss some new avenues of research that will complement these studies in the coming years.
Additional Links: PMID-33622103
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@article {pmid33622103,
year = {2021},
author = {Ros-Rocher, N and Pérez-Posada, A and Leger, MM and Ruiz-Trillo, I},
title = {The origin of animals: an ancestral reconstruction of the unicellular-to-multicellular transition.},
journal = {Open biology},
volume = {11},
number = {2},
pages = {200359},
doi = {10.1098/rsob.200359},
pmid = {33622103},
issn = {2046-2441},
abstract = {How animals evolved from a single-celled ancestor, transitioning from a unicellular lifestyle to a coordinated multicellular entity, remains a fascinating question. Key events in this transition involved the emergence of processes related to cell adhesion, cell-cell communication and gene regulation. To understand how these capacities evolved, we need to reconstruct the features of both the last common multicellular ancestor of animals and the last unicellular ancestor of animals. In this review, we summarize recent advances in the characterization of these ancestors, inferred by comparative genomic analyses between the earliest branching animals and those radiating later, and between animals and their closest unicellular relatives. We also provide an updated hypothesis regarding the transition to animal multicellularity, which was likely gradual and involved the use of gene regulatory mechanisms in the emergence of early developmental and morphogenetic plans. Finally, we discuss some new avenues of research that will complement these studies in the coming years.},
}
RevDate: 2021-02-23
CmpDate: 2021-02-23
Reverse-genetics studies of lncRNAs-what we have learnt and paths forward.
Genome biology, 21(1):93.
Long non-coding RNAs (lncRNAs) represent a major fraction of the transcriptome in multicellular organisms. Although a handful of well-studied lncRNAs are broadly recognized as biologically meaningful, the fraction of such transcripts out of the entire collection of lncRNAs remains a subject of vigorous debate. Here we review the evidence for and against biological functionalities of lncRNAs and attempt to arrive at potential modes of lncRNA functionality that would reconcile the contradictory conclusions. Finally, we discuss different strategies of phenotypic analyses that could be used to investigate such modes of lncRNA functionality.
Additional Links: PMID-32290841
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@article {pmid32290841,
year = {2020},
author = {Gao, F and Cai, Y and Kapranov, P and Xu, D},
title = {Reverse-genetics studies of lncRNAs-what we have learnt and paths forward.},
journal = {Genome biology},
volume = {21},
number = {1},
pages = {93},
pmid = {32290841},
issn = {1474-760X},
mesh = {Animals ; Evolution, Molecular ; Phenotype ; RNA, Long Noncoding/*physiology ; Reverse Genetics ; Vertebrates/genetics ; },
abstract = {Long non-coding RNAs (lncRNAs) represent a major fraction of the transcriptome in multicellular organisms. Although a handful of well-studied lncRNAs are broadly recognized as biologically meaningful, the fraction of such transcripts out of the entire collection of lncRNAs remains a subject of vigorous debate. Here we review the evidence for and against biological functionalities of lncRNAs and attempt to arrive at potential modes of lncRNA functionality that would reconcile the contradictory conclusions. Finally, we discuss different strategies of phenotypic analyses that could be used to investigate such modes of lncRNA functionality.},
}
MeSH Terms:
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Animals
Evolution, Molecular
Phenotype
RNA, Long Noncoding/*physiology
Reverse Genetics
Vertebrates/genetics
RevDate: 2021-02-19
Phloem Sap Proteins Are Part of a Core Stress Responsive Proteome Involved in Drought Stress Adjustment.
Frontiers in plant science, 12:625224.
During moderate drought stress, plants can adjust by changes in the protein profiles of the different organs. Plants transport and modulate extracellular stimuli local and systemically through commonly induced inter- and intracellular reactions. However, most proteins are frequently considered, cell and organelle specific. Hence, while signaling molecules and peptides can travel systemically throughout the whole plant, it is not clear, whether protein isoforms may exist ubiquitously across organs, and what function those may have during drought regulation. By applying shotgun proteomics, we extracted a core proteome of 92 identical protein isoforms, shared ubiquitously amongst several Medicago truncatula tissues, including roots, phloem sap, petioles, and leaves. We investigated their relative distribution across the different tissues and their response to moderate drought stress. In addition, we functionally compared this plant core stress responsive proteome with the organ-specific proteomes. Our study revealed plant ubiquitous protein isoforms, mainly related to redox homeostasis and signaling and involved in protein interaction networks across the whole plant. Furthermore, about 90% of these identified core protein isoforms were significantly involved in drought stress response, indicating a crucial role of the core stress responsive proteome (CSRP) in the plant organ cross-communication, important for a long-distance stress-responsive network. Besides, the data allowed for a comprehensive characterization of the phloem proteome, revealing new insights into its function. For instance, CSRP protein levels involved in stress and redox are relatively more abundant in the phloem compared to the other tissues already under control conditions. This suggests a major role of the phloem in stress protection and antioxidant activity enabling the plants metabolic maintenance and rapid response upon moderate stress. We anticipate our study to be a starting point for future investigations of the role of the core plant proteome. Under an evolutionary perspective, CSRP would enable communication of different cells with each other and the environment being crucial for coordinated stress response of multicellular organisms.
Additional Links: PMID-33603764
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@article {pmid33603764,
year = {2021},
author = {Castañeda, V and González, EM and Wienkoop, S},
title = {Phloem Sap Proteins Are Part of a Core Stress Responsive Proteome Involved in Drought Stress Adjustment.},
journal = {Frontiers in plant science},
volume = {12},
number = {},
pages = {625224},
doi = {10.3389/fpls.2021.625224},
pmid = {33603764},
issn = {1664-462X},
abstract = {During moderate drought stress, plants can adjust by changes in the protein profiles of the different organs. Plants transport and modulate extracellular stimuli local and systemically through commonly induced inter- and intracellular reactions. However, most proteins are frequently considered, cell and organelle specific. Hence, while signaling molecules and peptides can travel systemically throughout the whole plant, it is not clear, whether protein isoforms may exist ubiquitously across organs, and what function those may have during drought regulation. By applying shotgun proteomics, we extracted a core proteome of 92 identical protein isoforms, shared ubiquitously amongst several Medicago truncatula tissues, including roots, phloem sap, petioles, and leaves. We investigated their relative distribution across the different tissues and their response to moderate drought stress. In addition, we functionally compared this plant core stress responsive proteome with the organ-specific proteomes. Our study revealed plant ubiquitous protein isoforms, mainly related to redox homeostasis and signaling and involved in protein interaction networks across the whole plant. Furthermore, about 90% of these identified core protein isoforms were significantly involved in drought stress response, indicating a crucial role of the core stress responsive proteome (CSRP) in the plant organ cross-communication, important for a long-distance stress-responsive network. Besides, the data allowed for a comprehensive characterization of the phloem proteome, revealing new insights into its function. For instance, CSRP protein levels involved in stress and redox are relatively more abundant in the phloem compared to the other tissues already under control conditions. This suggests a major role of the phloem in stress protection and antioxidant activity enabling the plants metabolic maintenance and rapid response upon moderate stress. We anticipate our study to be a starting point for future investigations of the role of the core plant proteome. Under an evolutionary perspective, CSRP would enable communication of different cells with each other and the environment being crucial for coordinated stress response of multicellular organisms.},
}
RevDate: 2021-02-19
A developmental perspective of homology and evolutionary novelty.
Current topics in developmental biology, 141:1-38.
The development and evolution of multicellular body plans is complex. Many distinct organs and body parts must be reproduced at each generation, and those that are traceable over long time scales are considered homologous. Among the most pressing and least understood phenomena in evolutionary biology is the mode by which new homologs, or "novelties" are introduced to the body plan and whether the developmental changes associated with such evolution deserve special treatment. In this chapter, we address the concepts of homology and evolutionary novelty through the lens of development. We present a series of case studies, within insects and vertebrates, from which we propose a developmental model of multicellular organ identity. With this model in hand, we make predictions regarding the developmental evolution of body plans and highlight the need for more integrative analysis of developing systems.
Additional Links: PMID-33602485
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@article {pmid33602485,
year = {2021},
author = {McKenna, KZ and Wagner, GP and Cooper, KL},
title = {A developmental perspective of homology and evolutionary novelty.},
journal = {Current topics in developmental biology},
volume = {141},
number = {},
pages = {1-38},
doi = {10.1016/bs.ctdb.2020.12.001},
pmid = {33602485},
issn = {1557-8933},
abstract = {The development and evolution of multicellular body plans is complex. Many distinct organs and body parts must be reproduced at each generation, and those that are traceable over long time scales are considered homologous. Among the most pressing and least understood phenomena in evolutionary biology is the mode by which new homologs, or "novelties" are introduced to the body plan and whether the developmental changes associated with such evolution deserve special treatment. In this chapter, we address the concepts of homology and evolutionary novelty through the lens of development. We present a series of case studies, within insects and vertebrates, from which we propose a developmental model of multicellular organ identity. With this model in hand, we make predictions regarding the developmental evolution of body plans and highlight the need for more integrative analysis of developing systems.},
}
RevDate: 2021-02-17
Evidence for reduced immune gene diversity and activity during the evolution of termites.
Proceedings. Biological sciences, 288(1945):20203168.
The evolution of biological complexity is associated with the emergence of bespoke immune systems that maintain and protect organism integrity. Unlike the well-studied immune systems of cells and individuals, little is known about the origins of immunity during the transition to eusociality, a major evolutionary transition comparable to the evolution of multicellular organisms from single-celled ancestors. We aimed to tackle this by characterizing the immune gene repertoire of 18 cockroach and termite species, spanning the spectrum of solitary, subsocial and eusocial lifestyles. We find that key transitions in termite sociality are correlated with immune gene family contractions. In cross-species comparisons of immune gene expression, we find evidence for a caste-specific social defence system in termites, which appears to operate at the expense of individual immune protection. Our study indicates that a major transition in organismal complexity may have entailed a fundamental reshaping of the immune system optimized for group over individual defence.
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@article {pmid33593190,
year = {2021},
author = {He, S and Sieksmeyer, T and Che, Y and Mora, MAE and Stiblik, P and Banasiak, R and Harrison, MC and Šobotník, J and Wang, Z and Johnston, PR and McMahon, DP},
title = {Evidence for reduced immune gene diversity and activity during the evolution of termites.},
journal = {Proceedings. Biological sciences},
volume = {288},
number = {1945},
pages = {20203168},
doi = {10.1098/rspb.2020.3168},
pmid = {33593190},
issn = {1471-2954},
abstract = {The evolution of biological complexity is associated with the emergence of bespoke immune systems that maintain and protect organism integrity. Unlike the well-studied immune systems of cells and individuals, little is known about the origins of immunity during the transition to eusociality, a major evolutionary transition comparable to the evolution of multicellular organisms from single-celled ancestors. We aimed to tackle this by characterizing the immune gene repertoire of 18 cockroach and termite species, spanning the spectrum of solitary, subsocial and eusocial lifestyles. We find that key transitions in termite sociality are correlated with immune gene family contractions. In cross-species comparisons of immune gene expression, we find evidence for a caste-specific social defence system in termites, which appears to operate at the expense of individual immune protection. Our study indicates that a major transition in organismal complexity may have entailed a fundamental reshaping of the immune system optimized for group over individual defence.},
}
RevDate: 2021-02-12
A New Mathematical Model for Controlling Tumor Growth Based on Microenvironment Acidity and Oxygen Concentration.
BioMed research international, 2021:8886050.
Hypoxia and the pH level of the tumor microenvironment have a great impact on the treatment of tumors. Here, the tumor growth is controlled by regulating the oxygen concentration and the acidity of the tumor microenvironment by introducing a two-dimensional multiscale cellular automata model of avascular tumor growth. The spatiotemporal evolution of tumor growth and metabolic variations is modeled based on biological assumptions, physical structure, states of cells, and transition rules. Each cell is allocated to one of the following states: proliferating cancer, nonproliferating cancer, necrotic, and normal cells. According to the response of the microenvironmental conditions, each cell consumes/produces metabolic factors and updates its state based on some stochastic rules. The input parameters are compatible with cancer biology using experimental data. The effect of neighborhoods during mitosis and simulating spatial heterogeneity is studied by considering multicellular layer structure of tumor. A simple Darwinist mutation is considered by introducing a critical parameter (Nmm) that affects division probability of the proliferative tumor cells based on the microenvironmental conditions and cancer hallmarks. The results show that Nmm regulation has a significant influence on the dynamics of tumor growth, the growth fraction, necrotic fraction, and the concentration levels of the metabolic factors. The model not only is able to simulate the in vivo tumor growth quantitatively and qualitatively but also can simulate the concentration of metabolic factors, oxygen, and acidity graphically. The results show the spatial heterogeneity effects on the proliferation of cancer cells and the rest of the system. By increasing Nmm, tumor shrinkage and significant increasing in the oxygen concentration and the pH value of the tumor microenvironment are observed. The results demonstrate the model's ability, providing an essential tool for simulating different tumor evolution scenarios of a patient and reliable prediction of spatiotemporal progression of tumors for utilizing in personalized therapy.
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@article {pmid33575354,
year = {2021},
author = {Pourhasanzade, F and Sabzpoushan, SH},
title = {A New Mathematical Model for Controlling Tumor Growth Based on Microenvironment Acidity and Oxygen Concentration.},
journal = {BioMed research international},
volume = {2021},
number = {},
pages = {8886050},
doi = {10.1155/2021/8886050},
pmid = {33575354},
issn = {2314-6141},
abstract = {Hypoxia and the pH level of the tumor microenvironment have a great impact on the treatment of tumors. Here, the tumor growth is controlled by regulating the oxygen concentration and the acidity of the tumor microenvironment by introducing a two-dimensional multiscale cellular automata model of avascular tumor growth. The spatiotemporal evolution of tumor growth and metabolic variations is modeled based on biological assumptions, physical structure, states of cells, and transition rules. Each cell is allocated to one of the following states: proliferating cancer, nonproliferating cancer, necrotic, and normal cells. According to the response of the microenvironmental conditions, each cell consumes/produces metabolic factors and updates its state based on some stochastic rules. The input parameters are compatible with cancer biology using experimental data. The effect of neighborhoods during mitosis and simulating spatial heterogeneity is studied by considering multicellular layer structure of tumor. A simple Darwinist mutation is considered by introducing a critical parameter (Nmm) that affects division probability of the proliferative tumor cells based on the microenvironmental conditions and cancer hallmarks. The results show that Nmm regulation has a significant influence on the dynamics of tumor growth, the growth fraction, necrotic fraction, and the concentration levels of the metabolic factors. The model not only is able to simulate the in vivo tumor growth quantitatively and qualitatively but also can simulate the concentration of metabolic factors, oxygen, and acidity graphically. The results show the spatial heterogeneity effects on the proliferation of cancer cells and the rest of the system. By increasing Nmm, tumor shrinkage and significant increasing in the oxygen concentration and the pH value of the tumor microenvironment are observed. The results demonstrate the model's ability, providing an essential tool for simulating different tumor evolution scenarios of a patient and reliable prediction of spatiotemporal progression of tumors for utilizing in personalized therapy.},
}
RevDate: 2021-02-09
The actin networks of chytrid fungi reveal evolutionary loss of cytoskeletal complexity in the fungal kingdom.
Current biology : CB pii:S0960-9822(21)00001-4 [Epub ahead of print].
Cells from across the eukaryotic tree use actin polymer networks for a wide variety of functions, including endocytosis, cytokinesis, and cell migration. Despite this functional conservation, the actin cytoskeleton has undergone significant diversification, highlighted by the differences in the actin networks of mammalian cells and yeast. Chytrid fungi diverged before the emergence of the Dikarya (multicellular fungi and yeast) and therefore provide a unique opportunity to study actin cytoskeletal evolution. Chytrids have two life stages: zoospore cells that can swim with a flagellum and sessile sporangial cells that, like multicellular fungi, are encased in a chitinous cell wall. Here, we show that zoospores of the amphibian-killing chytrid Batrachochytrium dendrobatidis (Bd) build dynamic actin structures resembling those of animal cells, including an actin cortex, pseudopods, and filopodia-like spikes. In contrast, Bd sporangia assemble perinuclear actin shells and actin patches similar to those of yeast. The use of specific small-molecule inhibitors indicate that nearly all of Bd's actin structures are dynamic and use distinct nucleators: although pseudopods and actin patches are Arp2/3 dependent, the actin cortex appears formin dependent and actin spikes require both nucleators. Our analysis of multiple chytrid genomes reveals actin regulators and myosin motors found in animals, but not dikaryotic fungi, as well as fungal-specific components. The presence of animal- and yeast-like actin cytoskeletal components in the genome combined with the intermediate actin phenotypes in Bd suggests that the simplicity of the yeast cytoskeleton may be due to evolutionary loss.
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@article {pmid33561386,
year = {2021},
author = {Prostak, SM and Robinson, KA and Titus, MA and Fritz-Laylin, LK},
title = {The actin networks of chytrid fungi reveal evolutionary loss of cytoskeletal complexity in the fungal kingdom.},
journal = {Current biology : CB},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cub.2021.01.001},
pmid = {33561386},
issn = {1879-0445},
abstract = {Cells from across the eukaryotic tree use actin polymer networks for a wide variety of functions, including endocytosis, cytokinesis, and cell migration. Despite this functional conservation, the actin cytoskeleton has undergone significant diversification, highlighted by the differences in the actin networks of mammalian cells and yeast. Chytrid fungi diverged before the emergence of the Dikarya (multicellular fungi and yeast) and therefore provide a unique opportunity to study actin cytoskeletal evolution. Chytrids have two life stages: zoospore cells that can swim with a flagellum and sessile sporangial cells that, like multicellular fungi, are encased in a chitinous cell wall. Here, we show that zoospores of the amphibian-killing chytrid Batrachochytrium dendrobatidis (Bd) build dynamic actin structures resembling those of animal cells, including an actin cortex, pseudopods, and filopodia-like spikes. In contrast, Bd sporangia assemble perinuclear actin shells and actin patches similar to those of yeast. The use of specific small-molecule inhibitors indicate that nearly all of Bd's actin structures are dynamic and use distinct nucleators: although pseudopods and actin patches are Arp2/3 dependent, the actin cortex appears formin dependent and actin spikes require both nucleators. Our analysis of multiple chytrid genomes reveals actin regulators and myosin motors found in animals, but not dikaryotic fungi, as well as fungal-specific components. The presence of animal- and yeast-like actin cytoskeletal components in the genome combined with the intermediate actin phenotypes in Bd suggests that the simplicity of the yeast cytoskeleton may be due to evolutionary loss.},
}
RevDate: 2021-02-08
Reafference and the origin of the self in early nervous system evolution.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 376(1821):20190764.
Discussions of the function of early nervous systems usually focus on a causal flow from sensors to effectors, by which an animal coordinates its actions with exogenous changes in its environment. We propose, instead, that much early sensing was reafferent; it was responsive to the consequences of the animal's own actions. We distinguish two general categories of reafference-translocational and deformational-and use these to survey the distribution of several often-neglected forms of sensing, including gravity sensing, flow sensing and proprioception. We discuss sensing of these kinds in sponges, ctenophores, placozoans, cnidarians and bilaterians. Reafference is ubiquitous, as ongoing action, especially whole-body motility, will almost inevitably influence the senses. Corollary discharge-a pathway or circuit by which an animal tracks its own actions and their reafferent consequences-is not a necessary feature of reafferent sensing but a later-evolving mechanism. We also argue for the importance of reafferent sensing to the evolution of the body-self, a form of organization that enables an animal to sense and act as a single unit. This article is part of the theme issue 'Basal cognition: multicellularity, neurons and the cognitive lens'.
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@article {pmid33550954,
year = {2021},
author = {Jékely, G and Godfrey-Smith, P and Keijzer, F},
title = {Reafference and the origin of the self in early nervous system evolution.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {376},
number = {1821},
pages = {20190764},
doi = {10.1098/rstb.2019.0764},
pmid = {33550954},
issn = {1471-2970},
abstract = {Discussions of the function of early nervous systems usually focus on a causal flow from sensors to effectors, by which an animal coordinates its actions with exogenous changes in its environment. We propose, instead, that much early sensing was reafferent; it was responsive to the consequences of the animal's own actions. We distinguish two general categories of reafference-translocational and deformational-and use these to survey the distribution of several often-neglected forms of sensing, including gravity sensing, flow sensing and proprioception. We discuss sensing of these kinds in sponges, ctenophores, placozoans, cnidarians and bilaterians. Reafference is ubiquitous, as ongoing action, especially whole-body motility, will almost inevitably influence the senses. Corollary discharge-a pathway or circuit by which an animal tracks its own actions and their reafferent consequences-is not a necessary feature of reafferent sensing but a later-evolving mechanism. We also argue for the importance of reafferent sensing to the evolution of the body-self, a form of organization that enables an animal to sense and act as a single unit. This article is part of the theme issue 'Basal cognition: multicellularity, neurons and the cognitive lens'.},
}
RevDate: 2021-02-08
Bistability of somatic pattern memories: stochastic outcomes in bioelectric circuits underlying regeneration.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 376(1821):20190765.
Nervous systems' computational abilities are an evolutionary innovation, specializing and speed-optimizing ancient biophysical dynamics. Bioelectric signalling originated in cells' communication with the outside world and with each other, enabling cooperation towards adaptive construction and repair of multicellular bodies. Here, we review the emerging field of developmental bioelectricity, which links the field of basal cognition to state-of-the-art questions in regenerative medicine, synthetic bioengineering and even artificial intelligence. One of the predictions of this view is that regeneration and regulative development can restore correct large-scale anatomies from diverse starting states because, like the brain, they exploit bioelectric encoding of distributed goal states-in this case, pattern memories. We propose a new interpretation of recent stochastic regenerative phenotypes in planaria, by appealing to computational models of memory representation and processing in the brain. Moreover, we discuss novel findings showing that bioelectric changes induced in planaria can be stored in tissue for over a week, thus revealing that somatic bioelectric circuits in vivo can implement a long-term, re-writable memory medium. A consideration of the mechanisms, evolution and functionality of basal cognition makes novel predictions and provides an integrative perspective on the evolution, physiology and biomedicine of information processing in vivo. This article is part of the theme issue 'Basal cognition: multicellularity, neurons and the cognitive lens'.
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@article {pmid33550952,
year = {2021},
author = {Pezzulo, G and LaPalme, J and Durant, F and Levin, M},
title = {Bistability of somatic pattern memories: stochastic outcomes in bioelectric circuits underlying regeneration.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {376},
number = {1821},
pages = {20190765},
doi = {10.1098/rstb.2019.0765},
pmid = {33550952},
issn = {1471-2970},
abstract = {Nervous systems' computational abilities are an evolutionary innovation, specializing and speed-optimizing ancient biophysical dynamics. Bioelectric signalling originated in cells' communication with the outside world and with each other, enabling cooperation towards adaptive construction and repair of multicellular bodies. Here, we review the emerging field of developmental bioelectricity, which links the field of basal cognition to state-of-the-art questions in regenerative medicine, synthetic bioengineering and even artificial intelligence. One of the predictions of this view is that regeneration and regulative development can restore correct large-scale anatomies from diverse starting states because, like the brain, they exploit bioelectric encoding of distributed goal states-in this case, pattern memories. We propose a new interpretation of recent stochastic regenerative phenotypes in planaria, by appealing to computational models of memory representation and processing in the brain. Moreover, we discuss novel findings showing that bioelectric changes induced in planaria can be stored in tissue for over a week, thus revealing that somatic bioelectric circuits in vivo can implement a long-term, re-writable memory medium. A consideration of the mechanisms, evolution and functionality of basal cognition makes novel predictions and provides an integrative perspective on the evolution, physiology and biomedicine of information processing in vivo. This article is part of the theme issue 'Basal cognition: multicellularity, neurons and the cognitive lens'.},
}
RevDate: 2021-02-08
Choanoflagellates and the ancestry of neurosecretory vesicles.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 376(1821):20190759.
Neurosecretory vesicles are highly specialized trafficking organelles that store neurotransmitters that are released at presynaptic nerve endings and are, therefore, important for animal cell-cell signalling. Despite considerable anatomical and functional diversity of neurons in animals, the protein composition of neurosecretory vesicles in bilaterians appears to be similar. This similarity points towards a common evolutionary origin. Moreover, many putative homologues of key neurosecretory vesicle proteins predate the origin of the first neurons, and some even the origin of the first animals. However, little is known about the molecular toolkit of these vesicles in non-bilaterian animals and their closest unicellular relatives, making inferences about the evolutionary origin of neurosecretory vesicles extremely difficult. By comparing 28 proteins of the core neurosecretory vesicle proteome in 13 different species, we demonstrate that most of the proteins are present in unicellular organisms. Surprisingly, we find that the vesicular membrane-associated soluble N-ethylmaleimide-sensitive factor attachment protein receptor protein synaptobrevin is localized to the vesicle-rich apical and basal pole in the choanoflagellate Salpingoeca rosetta. Our 3D vesicle reconstructions reveal that the choanoflagellates S. rosetta and Monosiga brevicollis exhibit a polarized and diverse vesicular landscape reminiscent of the polarized organization of chemical synapses that secrete the content of neurosecretory vesicles into the synaptic cleft. This study sheds light on the ancestral molecular machinery of neurosecretory vesicles and provides a framework to understand the origin and evolution of secretory cells, synapses and neurons. This article is part of the theme issue 'Basal cognition: multicellularity, neurons and the cognitive lens'.
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@article {pmid33550951,
year = {2021},
author = {Göhde, R and Naumann, B and Laundon, D and Imig, C and McDonald, K and Cooper, BH and Varoqueaux, F and Fasshauer, D and Burkhardt, P},
title = {Choanoflagellates and the ancestry of neurosecretory vesicles.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {376},
number = {1821},
pages = {20190759},
doi = {10.1098/rstb.2019.0759},
pmid = {33550951},
issn = {1471-2970},
abstract = {Neurosecretory vesicles are highly specialized trafficking organelles that store neurotransmitters that are released at presynaptic nerve endings and are, therefore, important for animal cell-cell signalling. Despite considerable anatomical and functional diversity of neurons in animals, the protein composition of neurosecretory vesicles in bilaterians appears to be similar. This similarity points towards a common evolutionary origin. Moreover, many putative homologues of key neurosecretory vesicle proteins predate the origin of the first neurons, and some even the origin of the first animals. However, little is known about the molecular toolkit of these vesicles in non-bilaterian animals and their closest unicellular relatives, making inferences about the evolutionary origin of neurosecretory vesicles extremely difficult. By comparing 28 proteins of the core neurosecretory vesicle proteome in 13 different species, we demonstrate that most of the proteins are present in unicellular organisms. Surprisingly, we find that the vesicular membrane-associated soluble N-ethylmaleimide-sensitive factor attachment protein receptor protein synaptobrevin is localized to the vesicle-rich apical and basal pole in the choanoflagellate Salpingoeca rosetta. Our 3D vesicle reconstructions reveal that the choanoflagellates S. rosetta and Monosiga brevicollis exhibit a polarized and diverse vesicular landscape reminiscent of the polarized organization of chemical synapses that secrete the content of neurosecretory vesicles into the synaptic cleft. This study sheds light on the ancestral molecular machinery of neurosecretory vesicles and provides a framework to understand the origin and evolution of secretory cells, synapses and neurons. This article is part of the theme issue 'Basal cognition: multicellularity, neurons and the cognitive lens'.},
}
RevDate: 2021-02-08
Neural versus alternative integrative systems: molecular insights into origins of neurotransmitters.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 376(1821):20190762.
Transmitter signalling is the universal chemical language of any nervous system, but little is known about its early evolution. Here, we summarize data about the distribution and functions of neurotransmitter systems in basal metazoans as well as outline hypotheses of their origins. We explore the scenario that neurons arose from genetically different populations of secretory cells capable of volume chemical transmission and integration of behaviours without canonical synapses. The closest representation of this primordial organization is currently found in Placozoa, disk-like animals with the simplest known cell composition but complex behaviours. We propose that injury-related signalling was the evolutionary predecessor for integrative functions of early transmitters such as nitric oxide, ATP, protons, glutamate and small peptides. By contrast, acetylcholine, dopamine, noradrenaline, octopamine, serotonin and histamine were recruited as canonical neurotransmitters relatively later in animal evolution, only in bilaterians. Ligand-gated ion channels often preceded the establishment of novel neurotransmitter systems. Moreover, lineage-specific diversification of neurotransmitter receptors occurred in parallel within Cnidaria and several bilaterian lineages, including acoels. In summary, ancestral diversification of secretory signal molecules provides unique chemical microenvironments for behaviour-driven innovations that pave the way to complex brain functions and elementary cognition. This article is part of the theme issue 'Basal cognition: multicellularity, neurons and the cognitive lens'.
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@article {pmid33550949,
year = {2021},
author = {Moroz, LL and Romanova, DY and Kohn, AB},
title = {Neural versus alternative integrative systems: molecular insights into origins of neurotransmitters.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {376},
number = {1821},
pages = {20190762},
doi = {10.1098/rstb.2019.0762},
pmid = {33550949},
issn = {1471-2970},
abstract = {Transmitter signalling is the universal chemical language of any nervous system, but little is known about its early evolution. Here, we summarize data about the distribution and functions of neurotransmitter systems in basal metazoans as well as outline hypotheses of their origins. We explore the scenario that neurons arose from genetically different populations of secretory cells capable of volume chemical transmission and integration of behaviours without canonical synapses. The closest representation of this primordial organization is currently found in Placozoa, disk-like animals with the simplest known cell composition but complex behaviours. We propose that injury-related signalling was the evolutionary predecessor for integrative functions of early transmitters such as nitric oxide, ATP, protons, glutamate and small peptides. By contrast, acetylcholine, dopamine, noradrenaline, octopamine, serotonin and histamine were recruited as canonical neurotransmitters relatively later in animal evolution, only in bilaterians. Ligand-gated ion channels often preceded the establishment of novel neurotransmitter systems. Moreover, lineage-specific diversification of neurotransmitter receptors occurred in parallel within Cnidaria and several bilaterian lineages, including acoels. In summary, ancestral diversification of secretory signal molecules provides unique chemical microenvironments for behaviour-driven innovations that pave the way to complex brain functions and elementary cognition. This article is part of the theme issue 'Basal cognition: multicellularity, neurons and the cognitive lens'.},
}
RevDate: 2021-02-08
Elementary nervous systems.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 376(1821):20200347.
The evolutionary origin of the nervous system has been a matter of long-standing debate. This is due to the different perspectives taken. Earlier studies addressed nervous system origins at the cellular level. They focused on the selective advantage of the first neuron in its local context, and considered vertical sensory-motor reflex arcs the first nervous system. Later studies emphasized the value of the nervous system at the tissue level. Rather than acting locally, early neurons were seen as part of an elementary nerve net that enabled the horizontal coordination of tissue movements. Opinions have also differed on the nature of effector cells. While most authors have favoured contractile systems, others see the key output of the incipient nervous system in the coordination of motile cilia, or the secretion of antimicrobial peptides. I will discuss these divergent views and explore how they can be validated by molecular and single-cell data. From this survey, possible consensus emerges: (i) the first manifestation of the nervous system likely was a nerve net, whereas specialized local circuits evolved later; (ii) different nerve nets may have evolved for the coordination of contractile or cilia-driven movements; (iii) all evolving nerve nets facilitated new forms of animal behaviour with increasing body size. This article is part of the theme issue 'Basal cognition: multicellularity, neurons and the cognitive lens'.
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@article {pmid33550948,
year = {2021},
author = {Arendt, D},
title = {Elementary nervous systems.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {376},
number = {1821},
pages = {20200347},
doi = {10.1098/rstb.2020.0347},
pmid = {33550948},
issn = {1471-2970},
abstract = {The evolutionary origin of the nervous system has been a matter of long-standing debate. This is due to the different perspectives taken. Earlier studies addressed nervous system origins at the cellular level. They focused on the selective advantage of the first neuron in its local context, and considered vertical sensory-motor reflex arcs the first nervous system. Later studies emphasized the value of the nervous system at the tissue level. Rather than acting locally, early neurons were seen as part of an elementary nerve net that enabled the horizontal coordination of tissue movements. Opinions have also differed on the nature of effector cells. While most authors have favoured contractile systems, others see the key output of the incipient nervous system in the coordination of motile cilia, or the secretion of antimicrobial peptides. I will discuss these divergent views and explore how they can be validated by molecular and single-cell data. From this survey, possible consensus emerges: (i) the first manifestation of the nervous system likely was a nerve net, whereas specialized local circuits evolved later; (ii) different nerve nets may have evolved for the coordination of contractile or cilia-driven movements; (iii) all evolving nerve nets facilitated new forms of animal behaviour with increasing body size. This article is part of the theme issue 'Basal cognition: multicellularity, neurons and the cognitive lens'.},
}
RevDate: 2021-02-08
The chemical brain hypothesis for the origin of nervous systems.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 376(1821):20190761.
In nervous systems, there are two main modes of transmission for the propagation of activity between cells. Synaptic transmission relies on close contact at chemical or electrical synapses while volume transmission is mediated by diffusible chemical signals and does not require direct contact. It is possible to wire complex neuronal networks by both chemical and synaptic transmission. Both types of networks are ubiquitous in nervous systems, leading to the question which of the two appeared first in evolution. This paper explores a scenario where chemically organized cellular networks appeared before synapses in evolution, a possibility supported by the presence of complex peptidergic signalling in all animals except sponges. Small peptides are ideally suited to link up cells into chemical networks. They have unlimited diversity, high diffusivity and high copy numbers derived from repetitive precursors. But chemical signalling is diffusion limited and becomes inefficient in larger bodies. To overcome this, peptidergic cells may have developed projections and formed synaptically connected networks tiling body surfaces and displaying synchronized activity with pulsatile peptide release. The advent of circulatory systems and neurohemal organs further reduced the constraint imposed on chemical signalling by diffusion. This could have contributed to the explosive radiation of peptidergic signalling systems in stem bilaterians. Neurosecretory centres in extant nervous systems are still predominantly chemically wired and coexist with the synaptic brain. This article is part of the theme issue 'Basal cognition: multicellularity, neurons and the cognitive lens'.
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@article {pmid33550946,
year = {2021},
author = {Jékely, G},
title = {The chemical brain hypothesis for the origin of nervous systems.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {376},
number = {1821},
pages = {20190761},
doi = {10.1098/rstb.2019.0761},
pmid = {33550946},
issn = {1471-2970},
abstract = {In nervous systems, there are two main modes of transmission for the propagation of activity between cells. Synaptic transmission relies on close contact at chemical or electrical synapses while volume transmission is mediated by diffusible chemical signals and does not require direct contact. It is possible to wire complex neuronal networks by both chemical and synaptic transmission. Both types of networks are ubiquitous in nervous systems, leading to the question which of the two appeared first in evolution. This paper explores a scenario where chemically organized cellular networks appeared before synapses in evolution, a possibility supported by the presence of complex peptidergic signalling in all animals except sponges. Small peptides are ideally suited to link up cells into chemical networks. They have unlimited diversity, high diffusivity and high copy numbers derived from repetitive precursors. But chemical signalling is diffusion limited and becomes inefficient in larger bodies. To overcome this, peptidergic cells may have developed projections and formed synaptically connected networks tiling body surfaces and displaying synchronized activity with pulsatile peptide release. The advent of circulatory systems and neurohemal organs further reduced the constraint imposed on chemical signalling by diffusion. This could have contributed to the explosive radiation of peptidergic signalling systems in stem bilaterians. Neurosecretory centres in extant nervous systems are still predominantly chemically wired and coexist with the synaptic brain. This article is part of the theme issue 'Basal cognition: multicellularity, neurons and the cognitive lens'.},
}
RevDate: 2021-02-05
Somatic deficiency causes reproductive parasitism in a fungus.
Nature communications, 12(1):783.
Some multicellular organisms can fuse because mergers potentially provide mutual benefits. However, experimental evolution in the fungus Neurospora crassa has demonstrated that free fusion of mycelia favours cheater lineages, but the mechanism and evolutionary dynamics of this exploitation are unknown. Here we show, paradoxically, that all convergently evolved cheater lineages have similar fusion deficiencies. These mutants are unable to initiate fusion but retain access to wild-type mycelia that fuse with them. This asymmetry reduces cheater-mutant contributions to somatic substrate-bound hyphal networks, but increases representation of their nuclei in the aerial reproductive hyphae. Cheaters only benefit when relatively rare and likely impose genetic load reminiscent of germline senescence. We show that the consequences of somatic fusion can be unequally distributed among fusion partners, with the passive non-fusing partner profiting more. We discuss how our findings may relate to the extensive variation in fusion frequency of fungi found in nature.
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@article {pmid33542245,
year = {2021},
author = {Grum-Grzhimaylo, AA and Bastiaans, E and van den Heuvel, J and Berenguer Millanes, C and Debets, AJM and Aanen, DK},
title = {Somatic deficiency causes reproductive parasitism in a fungus.},
journal = {Nature communications},
volume = {12},
number = {1},
pages = {783},
pmid = {33542245},
issn = {2041-1723},
abstract = {Some multicellular organisms can fuse because mergers potentially provide mutual benefits. However, experimental evolution in the fungus Neurospora crassa has demonstrated that free fusion of mycelia favours cheater lineages, but the mechanism and evolutionary dynamics of this exploitation are unknown. Here we show, paradoxically, that all convergently evolved cheater lineages have similar fusion deficiencies. These mutants are unable to initiate fusion but retain access to wild-type mycelia that fuse with them. This asymmetry reduces cheater-mutant contributions to somatic substrate-bound hyphal networks, but increases representation of their nuclei in the aerial reproductive hyphae. Cheaters only benefit when relatively rare and likely impose genetic load reminiscent of germline senescence. We show that the consequences of somatic fusion can be unequally distributed among fusion partners, with the passive non-fusing partner profiting more. We discuss how our findings may relate to the extensive variation in fusion frequency of fungi found in nature.},
}
RevDate: 2021-02-04
Metabolic Stress and Immunity: Nutrient-Sensing Kinases and Tryptophan Metabolism.
Advances in experimental medicine and biology, 1275:395-405.
The tryptophan catabolizing enzyme indoleamine 2,3-dioxygenase (IDO-1) has gained major attention due the immunoregulatory nature of this pathway. Both depletion of tryptophan concentrations as well as the accumulation of downstream metabolites are relevant for the mediation of the manifold consequences of increased tryptophan metabolism. Increased tryptophan catabolism is indicative for several chronic inflammatory disorders such as infections, autoimmune diseases or cancer. Low tryptophan availability is likely to be involved in the manifestation of a variety of comorbidities such as anemia, cachexia, depression and neurocognitive disturbances.Several nutrient sensing kinases are implicated in the downstream effects of dysregulated tryptophan metabolism. These include mechanisms that were conserved during evolution but have gained special features in multicellular eukaryotes, such as pathways regulated by eukaryotic translation initiation factor 2 (eIF-2)-alpha kinase (GCN2, also named general control nonderepressible 2 kinase), 5'-adenosine monophosphate (AMP)-activated protein kinase (AMPK) and target of rapamycin (TOR).The interplay between IDO-1 and above-mentioned pathway seems to be highly context dependent. A better understanding of the crosstalk is necessary to support the search for druggable targets for the treatment of inflammatory and autoimmune disorders.
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@article {pmid33539025,
year = {2021},
author = {Gostner, JM and Fuchs, D and Kurz, K},
title = {Metabolic Stress and Immunity: Nutrient-Sensing Kinases and Tryptophan Metabolism.},
journal = {Advances in experimental medicine and biology},
volume = {1275},
number = {},
pages = {395-405},
pmid = {33539025},
issn = {0065-2598},
abstract = {The tryptophan catabolizing enzyme indoleamine 2,3-dioxygenase (IDO-1) has gained major attention due the immunoregulatory nature of this pathway. Both depletion of tryptophan concentrations as well as the accumulation of downstream metabolites are relevant for the mediation of the manifold consequences of increased tryptophan metabolism. Increased tryptophan catabolism is indicative for several chronic inflammatory disorders such as infections, autoimmune diseases or cancer. Low tryptophan availability is likely to be involved in the manifestation of a variety of comorbidities such as anemia, cachexia, depression and neurocognitive disturbances.Several nutrient sensing kinases are implicated in the downstream effects of dysregulated tryptophan metabolism. These include mechanisms that were conserved during evolution but have gained special features in multicellular eukaryotes, such as pathways regulated by eukaryotic translation initiation factor 2 (eIF-2)-alpha kinase (GCN2, also named general control nonderepressible 2 kinase), 5'-adenosine monophosphate (AMP)-activated protein kinase (AMPK) and target of rapamycin (TOR).The interplay between IDO-1 and above-mentioned pathway seems to be highly context dependent. A better understanding of the crosstalk is necessary to support the search for druggable targets for the treatment of inflammatory and autoimmune disorders.},
}
RevDate: 2021-02-04
Melatonin and Cancer: A Polyhedral Network Where the Source Matters.
Antioxidants (Basel, Switzerland), 10(2): pii:antiox10020210.
Melatonin is one of the most phylogenetically conserved signals in biology. Although its original function was probably related to its antioxidant capacity, this indoleamine has been "adopted" by multicellular organisms as the "darkness signal" when secreted in a circadian manner and is acutely suppressed by light at night by the pineal gland. However, melatonin is also produced by other tissues, which constitute its extrapineal sources. Apart from its undisputed chronobiotic function, melatonin exerts antioxidant, immunomodulatory, pro-apoptotic, antiproliferative, and anti-angiogenic effects, with all these properties making it a powerful antitumor agent. Indeed, this activity has been demonstrated to be mediated by interfering with various cancer hallmarks, and different epidemiological studies have also linked light at night (melatonin suppression) with a higher incidence of different types of cancer. In 2007, the World Health Organization classified night shift work as a probable carcinogen due to circadian disruption, where melatonin plays a central role. Our aim is to review, from a global perspective, the role of melatonin both from pineal and extrapineal origin, as well as their possible interplay, as an intrinsic factor in the incidence, development, and progression of cancer. Particular emphasis will be placed not only on those mechanisms related to melatonin's antioxidant nature but also on the recently described novel roles of melatonin in microbiota and epigenetic regulation.
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@article {pmid33535472,
year = {2021},
author = {Bonmati-Carrion, MA and Tomas-Loba, A},
title = {Melatonin and Cancer: A Polyhedral Network Where the Source Matters.},
journal = {Antioxidants (Basel, Switzerland)},
volume = {10},
number = {2},
pages = {},
doi = {10.3390/antiox10020210},
pmid = {33535472},
issn = {2076-3921},
support = {20401/SF/17//Fundación Séneca/ ; 19899/GERM/15//Fundación Séneca/ ; RYC2018-025622-I//Ministerio de Ciencia, Innovación y Universidades/ ; BFERO2020.01//Fundación Fero/ ; LeonardoFellowship//Fundación BBVA/ ; RTI2018-093528-B-I00//Ministerio de Ciencia, Innovación y Universidades/ ; CB16/10/00239//Ministerio de Economía y Competitividad/ ; },
abstract = {Melatonin is one of the most phylogenetically conserved signals in biology. Although its original function was probably related to its antioxidant capacity, this indoleamine has been "adopted" by multicellular organisms as the "darkness signal" when secreted in a circadian manner and is acutely suppressed by light at night by the pineal gland. However, melatonin is also produced by other tissues, which constitute its extrapineal sources. Apart from its undisputed chronobiotic function, melatonin exerts antioxidant, immunomodulatory, pro-apoptotic, antiproliferative, and anti-angiogenic effects, with all these properties making it a powerful antitumor agent. Indeed, this activity has been demonstrated to be mediated by interfering with various cancer hallmarks, and different epidemiological studies have also linked light at night (melatonin suppression) with a higher incidence of different types of cancer. In 2007, the World Health Organization classified night shift work as a probable carcinogen due to circadian disruption, where melatonin plays a central role. Our aim is to review, from a global perspective, the role of melatonin both from pineal and extrapineal origin, as well as their possible interplay, as an intrinsic factor in the incidence, development, and progression of cancer. Particular emphasis will be placed not only on those mechanisms related to melatonin's antioxidant nature but also on the recently described novel roles of melatonin in microbiota and epigenetic regulation.},
}
RevDate: 2021-02-04
How Soon Hath Time… A History of Two "Seminal" Publications.
Cells, 10(2): pii:cells10020287.
This review documents the history of the two papers written half a century ago that relate to this special issue of Cells. The first, "Sperm competition and its evolutionary consequences in the insects" (Biological Reviews, 1970), stressed that sexual selection continues after ejaculation, resulting in many adaptations (e.g., postcopulatory guarding phases, copulatory plugs, seminal fluid components that modify female reproduction, and optimal ejaculation strategies), an aspect not considered by Darwin in his classic treatise of 1871. Sperm competition has subsequently been studied in many taxa, and post-copulatory sexual selection is now considered an important sequel to Darwinian pre-copulatory sexual selection. The second, "The origin and evolution of gamete dimorphism and the male-female phenomenon" (Journal of Theoretical Biology, 1972) showed how selection, based on gamete competition between individuals, can give rise to anisogamy in an isogamous broadcast spawning ancestor. This theory, which has subsequently been developed in various ways, is argued to form the most powerful explanation of why there are two sexes in most multicellular organisms. Together, the two papers have influenced our general understanding of the evolutionary differentiation of the two forms of gametic cells, and the divergence of sexual strategies between males and females under sexual selection.
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@article {pmid33535413,
year = {2021},
author = {Parker, GA},
title = {How Soon Hath Time… A History of Two "Seminal" Publications.},
journal = {Cells},
volume = {10},
number = {2},
pages = {},
doi = {10.3390/cells10020287},
pmid = {33535413},
issn = {2073-4409},
abstract = {This review documents the history of the two papers written half a century ago that relate to this special issue of Cells. The first, "Sperm competition and its evolutionary consequences in the insects" (Biological Reviews, 1970), stressed that sexual selection continues after ejaculation, resulting in many adaptations (e.g., postcopulatory guarding phases, copulatory plugs, seminal fluid components that modify female reproduction, and optimal ejaculation strategies), an aspect not considered by Darwin in his classic treatise of 1871. Sperm competition has subsequently been studied in many taxa, and post-copulatory sexual selection is now considered an important sequel to Darwinian pre-copulatory sexual selection. The second, "The origin and evolution of gamete dimorphism and the male-female phenomenon" (Journal of Theoretical Biology, 1972) showed how selection, based on gamete competition between individuals, can give rise to anisogamy in an isogamous broadcast spawning ancestor. This theory, which has subsequently been developed in various ways, is argued to form the most powerful explanation of why there are two sexes in most multicellular organisms. Together, the two papers have influenced our general understanding of the evolutionary differentiation of the two forms of gametic cells, and the divergence of sexual strategies between males and females under sexual selection.},
}
RevDate: 2021-02-02
Elevated temperature increases genome-wide selection on de novo mutations.
Proceedings. Biological sciences, 288(1944):20203094.
Adaptation in new environments depends on the amount of genetic variation available for evolution, and the efficacy by which natural selection discriminates among this variation. However, whether some ecological factors reveal more genetic variation, or impose stronger selection pressures than others, is typically not known. Here, we apply the enzyme kinetic theory to show that rising global temperatures are predicted to intensify natural selection throughout the genome by increasing the effects of DNA sequence variation on protein stability. We test this prediction by (i) estimating temperature-dependent fitness effects of induced mutations in seed beetles adapted to ancestral or elevated temperature, and (ii) calculate 100 paired selection estimates on mutations in benign versus stressful environments from unicellular and multicellular organisms. Environmental stress per se did not increase mean selection on de novo mutation, suggesting that the cost of adaptation does not generally increase in new ecological settings to which the organism is maladapted. However, elevated temperature increased the mean strength of selection on genome-wide polymorphism, signified by increases in both mutation load and mutational variance in fitness. These results have important implications for genetic diversity gradients and the rate and repeatability of evolution under climate change.
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@article {pmid33529558,
year = {2021},
author = {Berger, D and Stångberg, J and Baur, J and Walters, RJ},
title = {Elevated temperature increases genome-wide selection on de novo mutations.},
journal = {Proceedings. Biological sciences},
volume = {288},
number = {1944},
pages = {20203094},
doi = {10.1098/rspb.2020.3094},
pmid = {33529558},
issn = {1471-2954},
abstract = {Adaptation in new environments depends on the amount of genetic variation available for evolution, and the efficacy by which natural selection discriminates among this variation. However, whether some ecological factors reveal more genetic variation, or impose stronger selection pressures than others, is typically not known. Here, we apply the enzyme kinetic theory to show that rising global temperatures are predicted to intensify natural selection throughout the genome by increasing the effects of DNA sequence variation on protein stability. We test this prediction by (i) estimating temperature-dependent fitness effects of induced mutations in seed beetles adapted to ancestral or elevated temperature, and (ii) calculate 100 paired selection estimates on mutations in benign versus stressful environments from unicellular and multicellular organisms. Environmental stress per se did not increase mean selection on de novo mutation, suggesting that the cost of adaptation does not generally increase in new ecological settings to which the organism is maladapted. However, elevated temperature increased the mean strength of selection on genome-wide polymorphism, signified by increases in both mutation load and mutational variance in fitness. These results have important implications for genetic diversity gradients and the rate and repeatability of evolution under climate change.},
}
RevDate: 2021-02-01
Taphonomic experiments imply a possible link between the evolution of multicellularity and the fossilization potential of soft-bodied organisms.
Ecology and evolution, 11(2):1037-1056 pii:ECE37120.
The reliability of evolutionary reconstructions based on the fossil record critically depends on our knowledge of the factors affecting the fossilization of soft-bodied organisms. Despite considerable research effort, these factors are still poorly understood. In order to elucidate the main prerequisites for the preservation of soft-bodied organisms, we conducted long-term (1-5 years) taphonomic experiments with the model crustacean Artemia salina buried in five different sediments. The subsequent analysis of the carcasses and sediments revealed that, in our experimental settings, better preservation was associated with the fast deposition of aluminum and silicon on organic tissues. Other elements such as calcium, magnesium, and iron, which can also accumulate quickly on the carcasses, appear to be much less efficient in preventing decay. Next, we asked if the carcasses of uni- and multicellular organisms differ in their ability to accumulate aluminum ions on their surface. The experiments with the flagellate Euglena gracilis and the sponge Spongilla lacustris showed that aluminum ions are more readily deposited onto a multicellular body. This was further confirmed by the experiments with uni- and multicellular stages of the social ameba Dictyostelium discoideum. The results lead us to speculate that the evolution of cell adhesion molecules, which provide efficient cell-cell and cell-substrate binding, probably can explain the rich fossil record of soft-bodied animals, the comparatively poor fossil record of nonskeletal unicellular eukaryotes, and the explosive emergence of the Cambrian diversity of soft-bodied fossils.
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@article {pmid33520185,
year = {2021},
author = {Naimark, E and Kirpotin, D and Boeva, N and Gmoshinskiy, V and Kalinina, M and Lyupina, Y and Markov, A and Nikitin, M and Shokurov, A and Volkov, D},
title = {Taphonomic experiments imply a possible link between the evolution of multicellularity and the fossilization potential of soft-bodied organisms.},
journal = {Ecology and evolution},
volume = {11},
number = {2},
pages = {1037-1056},
doi = {10.1002/ece3.7120},
pmid = {33520185},
issn = {2045-7758},
abstract = {The reliability of evolutionary reconstructions based on the fossil record critically depends on our knowledge of the factors affecting the fossilization of soft-bodied organisms. Despite considerable research effort, these factors are still poorly understood. In order to elucidate the main prerequisites for the preservation of soft-bodied organisms, we conducted long-term (1-5 years) taphonomic experiments with the model crustacean Artemia salina buried in five different sediments. The subsequent analysis of the carcasses and sediments revealed that, in our experimental settings, better preservation was associated with the fast deposition of aluminum and silicon on organic tissues. Other elements such as calcium, magnesium, and iron, which can also accumulate quickly on the carcasses, appear to be much less efficient in preventing decay. Next, we asked if the carcasses of uni- and multicellular organisms differ in their ability to accumulate aluminum ions on their surface. The experiments with the flagellate Euglena gracilis and the sponge Spongilla lacustris showed that aluminum ions are more readily deposited onto a multicellular body. This was further confirmed by the experiments with uni- and multicellular stages of the social ameba Dictyostelium discoideum. The results lead us to speculate that the evolution of cell adhesion molecules, which provide efficient cell-cell and cell-substrate binding, probably can explain the rich fossil record of soft-bodied animals, the comparatively poor fossil record of nonskeletal unicellular eukaryotes, and the explosive emergence of the Cambrian diversity of soft-bodied fossils.},
}
RevDate: 2021-01-28
Novel insights: Dynamic foam cells derived from the macrophage in atherosclerosis.
Journal of cellular physiology [Epub ahead of print].
Atherosclerosis can be regarded as a chronic disease derived from the interaction between disordered lipoproteins and an unsuitable immune response. The evolution of foam cells is not only a significant pathological change in the early stage of atherosclerosis but also a key stage in the occurrence and development of atherosclerosis. The formation of foam cells is mainly caused by the imbalance among lipids uptake, lipids treatment, and reverse cholesterol transport. Although a large number of studies have summarized the source of foam cells and the mechanism of foam cells formation, we propose a new idea about foam cells in atherosclerosis. Rather than an isolated microenvironment, the macrophage multiple lipid uptake pathways, lipid internalization, lysosome, mitochondria, endoplasmic reticulum, neutral cholesterol ester hydrolase (NCEH), acyl-coenzyme A-cholesterol acyltransferase (ACAT), and reverse cholesterol transport are mutually influential, and form a dynamic process under multi-factor regulation. The macrophage takes on different uptake lipid statuses depending on multiple uptake pathways and intracellular lipids, lipid metabolites versus pro-inflammatory factors. Except for NCEH and ACAT, the lipid internalization of macrophages also depends on multicellular organelles including the lysosome, mitochondria, and endoplasmic reticulum, which are associated with each other. A dynamic balance between esterification and hydrolysis of cholesterol for macrophages is essential for physiology and pathology. Therefore, we propose that the foam cell in the process of atherosclerosis may be dynamic under multi-factor regulation, and collate this study to provide a holistic and dynamic idea of the foam cell.
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@article {pmid33507545,
year = {2021},
author = {Li, J and Meng, Q and Fu, Y and Yu, X and Ji, T and Chao, Y and Chen, Q and Li, Y and Bian, H},
title = {Novel insights: Dynamic foam cells derived from the macrophage in atherosclerosis.},
journal = {Journal of cellular physiology},
volume = {},
number = {},
pages = {},
doi = {10.1002/jcp.30300},
pmid = {33507545},
issn = {1097-4652},
support = {81774029//National Natural Science Foundation of China/ ; },
abstract = {Atherosclerosis can be regarded as a chronic disease derived from the interaction between disordered lipoproteins and an unsuitable immune response. The evolution of foam cells is not only a significant pathological change in the early stage of atherosclerosis but also a key stage in the occurrence and development of atherosclerosis. The formation of foam cells is mainly caused by the imbalance among lipids uptake, lipids treatment, and reverse cholesterol transport. Although a large number of studies have summarized the source of foam cells and the mechanism of foam cells formation, we propose a new idea about foam cells in atherosclerosis. Rather than an isolated microenvironment, the macrophage multiple lipid uptake pathways, lipid internalization, lysosome, mitochondria, endoplasmic reticulum, neutral cholesterol ester hydrolase (NCEH), acyl-coenzyme A-cholesterol acyltransferase (ACAT), and reverse cholesterol transport are mutually influential, and form a dynamic process under multi-factor regulation. The macrophage takes on different uptake lipid statuses depending on multiple uptake pathways and intracellular lipids, lipid metabolites versus pro-inflammatory factors. Except for NCEH and ACAT, the lipid internalization of macrophages also depends on multicellular organelles including the lysosome, mitochondria, and endoplasmic reticulum, which are associated with each other. A dynamic balance between esterification and hydrolysis of cholesterol for macrophages is essential for physiology and pathology. Therefore, we propose that the foam cell in the process of atherosclerosis may be dynamic under multi-factor regulation, and collate this study to provide a holistic and dynamic idea of the foam cell.},
}
RevDate: 2021-01-25
Linking single-cell decisions to collective behaviours in social bacteria.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 376(1820):20190755.
Social bacteria display complex behaviours whereby thousands of cells collectively and dramatically change their form and function in response to nutrient availability and changing environmental conditions. In this review, we focus on Myxococcus xanthus motility, which supports spectacular transitions based on prey availability across its life cycle. A large body of work suggests that these behaviours require sensory capacity implemented at the single-cell level. Focusing on recent genetic work on a core cellular pathway required for single-cell directional decisions, we argue that signal integration, multi-modal sensing and memory are at the root of decision making leading to multicellular behaviours. Hence, Myxococcus may be a powerful biological system to elucidate how cellular building blocks cooperate to form sensory multicellular assemblages, a possible origin of cognitive mechanisms in biological systems. This article is part of the theme issue 'Basal cognition: conceptual tools and the view from the single cell'.
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@article {pmid33487114,
year = {2021},
author = {Dinet, C and Michelot, A and Herrou, J and Mignot, T},
title = {Linking single-cell decisions to collective behaviours in social bacteria.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {376},
number = {1820},
pages = {20190755},
doi = {10.1098/rstb.2019.0755},
pmid = {33487114},
issn = {1471-2970},
abstract = {Social bacteria display complex behaviours whereby thousands of cells collectively and dramatically change their form and function in response to nutrient availability and changing environmental conditions. In this review, we focus on Myxococcus xanthus motility, which supports spectacular transitions based on prey availability across its life cycle. A large body of work suggests that these behaviours require sensory capacity implemented at the single-cell level. Focusing on recent genetic work on a core cellular pathway required for single-cell directional decisions, we argue that signal integration, multi-modal sensing and memory are at the root of decision making leading to multicellular behaviours. Hence, Myxococcus may be a powerful biological system to elucidate how cellular building blocks cooperate to form sensory multicellular assemblages, a possible origin of cognitive mechanisms in biological systems. This article is part of the theme issue 'Basal cognition: conceptual tools and the view from the single cell'.},
}
RevDate: 2021-01-25
From environmental sensing to developmental control: cognitive evolution in dictyostelid social amoebas.
Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 376(1820):20190756.
Dictyostelid social amoebas respond to starvation by self-organizing into multicellular slugs that migrate towards light to construct spore-bearing structures. These behaviours depend on excitable networks that enable amoebas to produce propagating waves of the chemoattractant cAMP, and to respond by directional movement. cAMP additionally regulates cell differentiation throughout development, with differentiation and cell movement being coordinated by interaction of the stalk inducer c-di-GMP with the adenylate cyclase that generates cAMP oscillations. Evolutionary studies indicate how the manifold roles of cAMP in multicellular development evolved from a role as intermediate for starvation-induced encystation in the unicellular ancestor. A merger of this stress response with the chemotaxis excitable networks yielded the developmental complexity and cognitive capabilities of extant Dictyostelia. This article is part of the theme issue 'Basal cognition: conceptual tools and the view from the single cell'.
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@article {pmid33487113,
year = {2021},
author = {Schaap, P},
title = {From environmental sensing to developmental control: cognitive evolution in dictyostelid social amoebas.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {376},
number = {1820},
pages = {20190756},
doi = {10.1098/rstb.2019.0756},
pmid = {33487113},
issn = {1471-2970},
abstract = {Dictyostelid social amoebas respond to starvation by self-organizing into multicellular slugs that migrate towards light to construct spore-bearing structures. These behaviours depend on excitable networks that enable amoebas to produce propagating waves of the chemoattractant cAMP, and to respond by directional movement. cAMP additionally regulates cell differentiation throughout development, with differentiation and cell movement being coordinated by interaction of the stalk inducer c-di-GMP with the adenylate cyclase that generates cAMP oscillations. Evolutionary studies indicate how the manifold roles of cAMP in multicellular development evolved from a role as intermediate for starvation-induced encystation in the unicellular ancestor. A merger of this stress response with the chemotaxis excitable networks yielded the developmental complexity and cognitive capabilities of extant Dictyostelia. This article is part of the theme issue 'Basal cognition: conceptual tools and the view from the single cell'.},
}
RevDate: 2021-01-22
Abundantly expressed class of noncoding RNAs conserved through the multicellular evolution of dictyostelid social amoebae.
Genome research pii:gr.272856.120 [Epub ahead of print].
Aggregative multicellularity has evolved multiple times in diverse groups of eukaryotes, exemplified by the well-studied development of dictyostelid social amoebae, e.g. Dictyostelium discoideum However, it is still poorly understood why multicellularity emerged in these amoebae while the great majority of other members of Amoebozoa are unicellular. Previously a novel type of noncoding RNA, Class I RNAs, was identified in D. discoideum and demonstrated to be important for normal multicellular development. Here we investigated Class I RNA evolution and its connection to multicellular development. We identified a large number of new Class I RNA genes by constructing a co-variance model combined with a scoring system based on conserved upstream sequences. Multiple genes were predicted in representatives of each major group of Dictyostelia and expression analysis confirmed that our search approach identifies expressed Class I RNA genes with high accuracy and sensitivity and that the RNAs are developmentally regulated. Further studies showed that Class I RNAs are ubiquitous in Dictyostelia and share highly conserved structure and sequence motifs. In addition, Class I RNA genes appear to be unique to dictyostelid social amoebae since they could not be identified in outgroup genomes, including their closest known relatives. Our results show that Class I RNA is an ancient class of ncRNAs, likely to have been present in the last common ancestor of Dictyostelia dating back at least 600 million years. Based on previous functional analyses and the presented evolutionary investigation, we hypothesize that Class I RNAs were involved in evolution of multicellularity in Dictyostelia.
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@article {pmid33479022,
year = {2021},
author = {Kjellin, J and Avesson, L and Reimegård, J and Liao, Z and Eichinger, L and Noegel, A and Glöckner, G and Schaap, P and Söderbom, F},
title = {Abundantly expressed class of noncoding RNAs conserved through the multicellular evolution of dictyostelid social amoebae.},
journal = {Genome research},
volume = {},
number = {},
pages = {},
doi = {10.1101/gr.272856.120},
pmid = {33479022},
issn = {1549-5469},
abstract = {Aggregative multicellularity has evolved multiple times in diverse groups of eukaryotes, exemplified by the well-studied development of dictyostelid social amoebae, e.g. Dictyostelium discoideum However, it is still poorly understood why multicellularity emerged in these amoebae while the great majority of other members of Amoebozoa are unicellular. Previously a novel type of noncoding RNA, Class I RNAs, was identified in D. discoideum and demonstrated to be important for normal multicellular development. Here we investigated Class I RNA evolution and its connection to multicellular development. We identified a large number of new Class I RNA genes by constructing a co-variance model combined with a scoring system based on conserved upstream sequences. Multiple genes were predicted in representatives of each major group of Dictyostelia and expression analysis confirmed that our search approach identifies expressed Class I RNA genes with high accuracy and sensitivity and that the RNAs are developmentally regulated. Further studies showed that Class I RNAs are ubiquitous in Dictyostelia and share highly conserved structure and sequence motifs. In addition, Class I RNA genes appear to be unique to dictyostelid social amoebae since they could not be identified in outgroup genomes, including their closest known relatives. Our results show that Class I RNA is an ancient class of ncRNAs, likely to have been present in the last common ancestor of Dictyostelia dating back at least 600 million years. Based on previous functional analyses and the presented evolutionary investigation, we hypothesize that Class I RNAs were involved in evolution of multicellularity in Dictyostelia.},
}
RevDate: 2021-01-20
Aggregative cycles evolve as a solution to conflicts in social investment.
PLoS computational biology, 17(1):e1008617 pii:PCOMPBIOL-D-20-01189 [Epub ahead of print].
Multicellular organization is particularly vulnerable to conflicts between different cell types when the body forms from initially isolated cells, as in aggregative multicellular microbes. Like other functions of the multicellular phase, coordinated collective movement can be undermined by conflicts between cells that spend energy in fuelling motion and 'cheaters' that get carried along. The evolutionary stability of collective behaviours against such conflicts is typically addressed in populations that undergo extrinsically imposed phases of aggregation and dispersal. Here, via a shift in perspective, we propose that aggregative multicellular cycles may have emerged as a way to temporally compartmentalize social conflicts. Through an eco-evolutionary mathematical model that accounts for individual and collective strategies of resource acquisition, we address regimes where different motility types coexist. Particularly interesting is the oscillatory regime that, similarly to life cycles of aggregative multicellular organisms, alternates on the timescale of several cell generations phases of prevalent solitary living and starvation-triggered aggregation. Crucially, such self-organized oscillations emerge as a result of evolution of cell traits associated to conflict escalation within multicellular aggregates.
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@article {pmid33471791,
year = {2021},
author = {Miele, L and De Monte, S},
title = {Aggregative cycles evolve as a solution to conflicts in social investment.},
journal = {PLoS computational biology},
volume = {17},
number = {1},
pages = {e1008617},
doi = {10.1371/journal.pcbi.1008617},
pmid = {33471791},
issn = {1553-7358},
abstract = {Multicellular organization is particularly vulnerable to conflicts between different cell types when the body forms from initially isolated cells, as in aggregative multicellular microbes. Like other functions of the multicellular phase, coordinated collective movement can be undermined by conflicts between cells that spend energy in fuelling motion and 'cheaters' that get carried along. The evolutionary stability of collective behaviours against such conflicts is typically addressed in populations that undergo extrinsically imposed phases of aggregation and dispersal. Here, via a shift in perspective, we propose that aggregative multicellular cycles may have emerged as a way to temporally compartmentalize social conflicts. Through an eco-evolutionary mathematical model that accounts for individual and collective strategies of resource acquisition, we address regimes where different motility types coexist. Particularly interesting is the oscillatory regime that, similarly to life cycles of aggregative multicellular organisms, alternates on the timescale of several cell generations phases of prevalent solitary living and starvation-triggered aggregation. Crucially, such self-organized oscillations emerge as a result of evolution of cell traits associated to conflict escalation within multicellular aggregates.},
}
RevDate: 2021-01-20
Neural stemness contributes to cell tumorigenicity.
Cell & bioscience, 11(1):21.
BACKGROUND: Previous studies demonstrated the dependence of cancer on nerve. Recently, a growing number of studies reveal that cancer cells share the property and regulatory network with neural stem/progenitor cells. However, relationship between the property of neural stemness and cell tumorigenicity is unknown.
RESULTS: We show that neural stem/progenitor cells, but not non-neural embryonic or somatic stem/progenitor cell types, exhibit tumorigenicity and the potential for differentiation into tissue types of all germ layers when they are placed in non-native environment by transplantation into immunodeficient nude mice. Likewise, cancer cells capable of tumor initiation have the property of neural stemness because of their abilities in neurosphere formation in neural stem cell-specific serum-free medium and in differentiation potential, in addition to their neuronal differentiation potential that was characterized previously. Moreover, loss of a pro-differentiation factor in myoblasts, which have no tumorigenicity, lead to the loss of myoblast identity, and gain of the property of neural stemness, tumorigenicity and potential for re-differentiation. By contrast, loss of neural stemness via differentiation results in the loss of tumorigenicity. These suggest that the property of neural stemness contributes to cell tumorigenicity, and tumor phenotypic heterogeneity might be an effect of differentiation potential of neural stemness. Bioinformatic analysis reveals that neural genes in general are correlated with embryonic development and cancer, in addition to their role in neural development; whereas non-neural genes are not. Most of neural specific genes emerged in typical species representing transition from unicellularity to multicellularity during evolution. Genes in Monosiga brevicollis, a unicellular species that is a closest known relative of metazoans, are biased toward neural cells.
CONCLUSIONS: We suggest that the property of neural stemness is the source of cell tumorigenicity. This is due to that neural biased unicellular state is the ground state for multicellularity and hence cell type diversification or differentiation during evolution, and tumorigenesis is a process of restoration of neural ground state in somatic cells along a default route that is pre-determined by an evolutionary advantage of neural state.
Additional Links: PMID-33468253
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@article {pmid33468253,
year = {2021},
author = {Xu, L and Zhang, M and Shi, L and Yang, X and Chen, L and Cao, N and Lei, A and Cao, Y},
title = {Neural stemness contributes to cell tumorigenicity.},
journal = {Cell & bioscience},
volume = {11},
number = {1},
pages = {21},
pmid = {33468253},
issn = {2045-3701},
support = {31671499//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: Previous studies demonstrated the dependence of cancer on nerve. Recently, a growing number of studies reveal that cancer cells share the property and regulatory network with neural stem/progenitor cells. However, relationship between the property of neural stemness and cell tumorigenicity is unknown.
RESULTS: We show that neural stem/progenitor cells, but not non-neural embryonic or somatic stem/progenitor cell types, exhibit tumorigenicity and the potential for differentiation into tissue types of all germ layers when they are placed in non-native environment by transplantation into immunodeficient nude mice. Likewise, cancer cells capable of tumor initiation have the property of neural stemness because of their abilities in neurosphere formation in neural stem cell-specific serum-free medium and in differentiation potential, in addition to their neuronal differentiation potential that was characterized previously. Moreover, loss of a pro-differentiation factor in myoblasts, which have no tumorigenicity, lead to the loss of myoblast identity, and gain of the property of neural stemness, tumorigenicity and potential for re-differentiation. By contrast, loss of neural stemness via differentiation results in the loss of tumorigenicity. These suggest that the property of neural stemness contributes to cell tumorigenicity, and tumor phenotypic heterogeneity might be an effect of differentiation potential of neural stemness. Bioinformatic analysis reveals that neural genes in general are correlated with embryonic development and cancer, in addition to their role in neural development; whereas non-neural genes are not. Most of neural specific genes emerged in typical species representing transition from unicellularity to multicellularity during evolution. Genes in Monosiga brevicollis, a unicellular species that is a closest known relative of metazoans, are biased toward neural cells.
CONCLUSIONS: We suggest that the property of neural stemness is the source of cell tumorigenicity. This is due to that neural biased unicellular state is the ground state for multicellularity and hence cell type diversification or differentiation during evolution, and tumorigenesis is a process of restoration of neural ground state in somatic cells along a default route that is pre-determined by an evolutionary advantage of neural state.},
}
RevDate: 2021-01-18
Early patterning of ABCB, ABCC, and ABCG transporters establishes unique territories of small molecule transport in the embryonic mesoderm and endoderm.
Developmental biology pii:S0012-1606(21)00006-3 [Epub ahead of print].
Directed intercellular movement of diverse small molecules, including metabolites, signal molecules and xenobiotics, is a key feature of multicellularity. Networks of small molecule transporters (SMTs), including several ATP Binding Cassette (ABC) transporters, are central to this process. While small molecule transporters are well described in differentiated organs, little is known about their patterns of expression in early embryogenesis. Here we report the pattern of ABC-type SMT expression and activity during the early development of sea urchins. Of the six major ABCs in this embryo (ABCB1, -B4, -C1, -C4, -C5 and -G2), three expression patterns were observed: 1) ABCB1 and ABCC1 are first expressed ubiquitously, and then become enriched in endoderm and ectoderm-derived structures. 2) ABCC4 and ABCC5 are restricted to a ring of mesoderm in the blastula and ABCC4 is later expressed in the coelomic pouches, the embryonic niche of the primordial germ cells. 3) ABCB4 and ABCG2 are expressed exclusively in endoderm-fated cells. Assays with fluorescent substrates and inhibitors of transporters revealed a ring of ABCC4 efflux activity emanating from ABCC4+ mesodermal cells. Similarly, ABCB1 and ABCB4 efflux activity was observed in the developing gut, prior to the onset of feeding. This study reveals the early establishment of unique territories of small molecule transport during embryogenesis. A pattern of ABCC4/C5 expression is consistent with signaling functions during gut invagination and germ line development, while a later pattern of ABCB1/B4 and ABCG2 is consistent with roles in the embryonic gut. This work provides a conceptual framework with which to examine the function and evolution of SMT networks and define the specific developmental pathways that drive the expression of these genes.
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@article {pmid33460641,
year = {2021},
author = {Schrankel, CS and Hamdoun, A},
title = {Early patterning of ABCB, ABCC, and ABCG transporters establishes unique territories of small molecule transport in the embryonic mesoderm and endoderm.},
journal = {Developmental biology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ydbio.2020.12.021},
pmid = {33460641},
issn = {1095-564X},
abstract = {Directed intercellular movement of diverse small molecules, including metabolites, signal molecules and xenobiotics, is a key feature of multicellularity. Networks of small molecule transporters (SMTs), including several ATP Binding Cassette (ABC) transporters, are central to this process. While small molecule transporters are well described in differentiated organs, little is known about their patterns of expression in early embryogenesis. Here we report the pattern of ABC-type SMT expression and activity during the early development of sea urchins. Of the six major ABCs in this embryo (ABCB1, -B4, -C1, -C4, -C5 and -G2), three expression patterns were observed: 1) ABCB1 and ABCC1 are first expressed ubiquitously, and then become enriched in endoderm and ectoderm-derived structures. 2) ABCC4 and ABCC5 are restricted to a ring of mesoderm in the blastula and ABCC4 is later expressed in the coelomic pouches, the embryonic niche of the primordial germ cells. 3) ABCB4 and ABCG2 are expressed exclusively in endoderm-fated cells. Assays with fluorescent substrates and inhibitors of transporters revealed a ring of ABCC4 efflux activity emanating from ABCC4+ mesodermal cells. Similarly, ABCB1 and ABCB4 efflux activity was observed in the developing gut, prior to the onset of feeding. This study reveals the early establishment of unique territories of small molecule transport during embryogenesis. A pattern of ABCC4/C5 expression is consistent with signaling functions during gut invagination and germ line development, while a later pattern of ABCB1/B4 and ABCG2 is consistent with roles in the embryonic gut. This work provides a conceptual framework with which to examine the function and evolution of SMT networks and define the specific developmental pathways that drive the expression of these genes.},
}
RevDate: 2021-01-15
Synthetic Lateral Inhibition in Periodic Pattern Forming Microbial Colonies.
ACS synthetic biology [Epub ahead of print].
Multicellular entities are characterized by intricate spatial patterns, intimately related to the functions they perform. These patterns are often created from isotropic embryonic structures, without external information cues guiding the symmetry breaking process. Mature biological structures also display characteristic scales with repeating distributions of signals or chemical species across space. Many candidate patterning modules have been used to explain processes during development and typically include a set of interacting and diffusing chemicals or agents known as morphogens. Great effort has been put forward to better understand the conditions in which pattern-forming processes can occur in the biological domain. However, evidence and practical knowledge allowing us to engineer symmetry-breaking is still lacking. Here we follow a different approach by designing a synthetic gene circuit in E. coli that implements a local activation long-range inhibition mechanism. The synthetic gene network implements an artificial differentiation process that changes the physicochemical properties of the agents. Using both experimental results and modeling, we show that the proposed system is capable of symmetry-breaking leading to regular spatial patterns during colony growth. Studying how these patterns emerge is fundamental to further our understanding of the evolution of biocomplexity and the role played by self-organization. The artificial system studied here and the engineering perspective on embryogenic processes can help validate developmental theories and identify universal properties underpinning biological pattern formation, with special interest for the area of synthetic developmental biology.
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@article {pmid33449631,
year = {2021},
author = {Duran-Nebreda, S and Pla, J and Vidiella, B and Piñero, J and Conde-Pueyo, N and Solé, R},
title = {Synthetic Lateral Inhibition in Periodic Pattern Forming Microbial Colonies.},
journal = {ACS synthetic biology},
volume = {},
number = {},
pages = {},
doi = {10.1021/acssynbio.0c00318},
pmid = {33449631},
issn = {2161-5063},
abstract = {Multicellular entities are characterized by intricate spatial patterns, intimately related to the functions they perform. These patterns are often created from isotropic embryonic structures, without external information cues guiding the symmetry breaking process. Mature biological structures also display characteristic scales with repeating distributions of signals or chemical species across space. Many candidate patterning modules have been used to explain processes during development and typically include a set of interacting and diffusing chemicals or agents known as morphogens. Great effort has been put forward to better understand the conditions in which pattern-forming processes can occur in the biological domain. However, evidence and practical knowledge allowing us to engineer symmetry-breaking is still lacking. Here we follow a different approach by designing a synthetic gene circuit in E. coli that implements a local activation long-range inhibition mechanism. The synthetic gene network implements an artificial differentiation process that changes the physicochemical properties of the agents. Using both experimental results and modeling, we show that the proposed system is capable of symmetry-breaking leading to regular spatial patterns during colony growth. Studying how these patterns emerge is fundamental to further our understanding of the evolution of biocomplexity and the role played by self-organization. The artificial system studied here and the engineering perspective on embryogenic processes can help validate developmental theories and identify universal properties underpinning biological pattern formation, with special interest for the area of synthetic developmental biology.},
}
RevDate: 2021-01-15
Phylodynamics for cell biologists.
Science (New York, N.Y.), 371(6526):.
Multicellular organisms are composed of cells connected by ancestry and descent from progenitor cells. The dynamics of cell birth, death, and inheritance within an organism give rise to the fundamental processes of development, differentiation, and cancer. Technical advances in molecular biology now allow us to study cellular composition, ancestry, and evolution at the resolution of individual cells within an organism or tissue. Here, we take a phylogenetic and phylodynamic approach to single-cell biology. We explain how "tree thinking" is important to the interpretation of the growing body of cell-level data and how ecological null models can benefit statistical hypothesis testing. Experimental progress in cell biology should be accompanied by theoretical developments if we are to exploit fully the dynamical information in single-cell data.
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@article {pmid33446527,
year = {2021},
author = {Stadler, T and Pybus, OG and Stumpf, MPH},
title = {Phylodynamics for cell biologists.},
journal = {Science (New York, N.Y.)},
volume = {371},
number = {6526},
pages = {},
doi = {10.1126/science.aah6266},
pmid = {33446527},
issn = {1095-9203},
abstract = {Multicellular organisms are composed of cells connected by ancestry and descent from progenitor cells. The dynamics of cell birth, death, and inheritance within an organism give rise to the fundamental processes of development, differentiation, and cancer. Technical advances in molecular biology now allow us to study cellular composition, ancestry, and evolution at the resolution of individual cells within an organism or tissue. Here, we take a phylogenetic and phylodynamic approach to single-cell biology. We explain how "tree thinking" is important to the interpretation of the growing body of cell-level data and how ecological null models can benefit statistical hypothesis testing. Experimental progress in cell biology should be accompanied by theoretical developments if we are to exploit fully the dynamical information in single-cell data.},
}
RevDate: 2021-01-14
Multiple Roles for Cholinergic Signaling from the Perspective of Stem Cell Function.
International journal of molecular sciences, 22(2): pii:ijms22020666.
Stem cells have extensive proliferative potential and the ability to differentiate into one or more mature cell types. The mechanisms by which stem cells accomplish self-renewal provide fundamental insight into the origin and design of multicellular organisms. These pathways allow the repair of damage and extend organismal life beyond that of component cells, and they probably preceded the evolution of complex metazoans. Understanding the true nature of stem cells can only come from discovering how they are regulated. The concept that stem cells are controlled by particular microenvironments, also known as niches, has been widely accepted. Technical advances now allow characterization of the zones that maintain and control stem cell activity in several organs, including the brain, skin, and gut. Cholinergic neurons release acetylcholine (ACh) that mediates chemical transmission via ACh receptors such as nicotinic and muscarinic receptors. Although the cholinergic system is composed of organized nerve cells, the system is also involved in mammalian non-neuronal cells, including stem cells, embryonic stem cells, epithelial cells, and endothelial cells. Thus, cholinergic signaling plays a pivotal role in controlling their behaviors. Studies regarding this signal are beginning to unify our understanding of stem cell regulation at the cellular and molecular levels, and they are expected to advance efforts to control stem cells therapeutically. The present article reviews recent findings about cholinergic signaling that is essential to control stem cell function in a cholinergic niche.
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@article {pmid33440882,
year = {2021},
author = {Takahashi, T},
title = {Multiple Roles for Cholinergic Signaling from the Perspective of Stem Cell Function.},
journal = {International journal of molecular sciences},
volume = {22},
number = {2},
pages = {},
doi = {10.3390/ijms22020666},
pmid = {33440882},
issn = {1422-0067},
support = {JP17K07495 and JP20K06751//Japan Society for the Promotion of Science/ ; },
abstract = {Stem cells have extensive proliferative potential and the ability to differentiate into one or more mature cell types. The mechanisms by which stem cells accomplish self-renewal provide fundamental insight into the origin and design of multicellular organisms. These pathways allow the repair of damage and extend organismal life beyond that of component cells, and they probably preceded the evolution of complex metazoans. Understanding the true nature of stem cells can only come from discovering how they are regulated. The concept that stem cells are controlled by particular microenvironments, also known as niches, has been widely accepted. Technical advances now allow characterization of the zones that maintain and control stem cell activity in several organs, including the brain, skin, and gut. Cholinergic neurons release acetylcholine (ACh) that mediates chemical transmission via ACh receptors such as nicotinic and muscarinic receptors. Although the cholinergic system is composed of organized nerve cells, the system is also involved in mammalian non-neuronal cells, including stem cells, embryonic stem cells, epithelial cells, and endothelial cells. Thus, cholinergic signaling plays a pivotal role in controlling their behaviors. Studies regarding this signal are beginning to unify our understanding of stem cell regulation at the cellular and molecular levels, and they are expected to advance efforts to control stem cells therapeutically. The present article reviews recent findings about cholinergic signaling that is essential to control stem cell function in a cholinergic niche.},
}
RevDate: 2021-01-14
Effects of Dysbiosis and Dietary Manipulation on the Digestive Microbiota of a Detritivorous Arthropod.
Microorganisms, 9(1): pii:microorganisms9010148.
The crucial role of microbes in the evolution, development, health, and ecological interactions of multicellular organisms is now widely recognized in the holobiont concept. However, the structure and stability of microbiota are highly dependent on abiotic and biotic factors, especially in the gut, which can be colonized by transient bacteria depending on the host's diet. We studied these impacts by manipulating the digestive microbiota of the detritivore Armadillidium vulgare and analyzing the consequences on its structure and function. Hosts were exposed to initial starvation and then were fed diets that varied the different components of lignocellulose. A total of 72 digestive microbiota were analyzed according to the type of the diet (standard or enriched in cellulose, lignin, or hemicellulose) and the period following dysbiosis. The results showed that microbiota from the hepatopancreas were very stable and resilient, while the most diverse and labile over time were found in the hindgut. Dysbiosis and selective diets may have affected the host fitness by altering the structure of the microbiota and its predicted functions. Overall, these modifications can therefore have effects not only on the holobiont, but also on the "eco-holobiont" conceptualization of macroorganisms.
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@article {pmid33440837,
year = {2021},
author = {Bredon, M and Depuydt, E and Brisson, L and Moulin, L and Charles, C and Haenn, S and Moumen, B and Bouchon, D},
title = {Effects of Dysbiosis and Dietary Manipulation on the Digestive Microbiota of a Detritivorous Arthropod.},
journal = {Microorganisms},
volume = {9},
number = {1},
pages = {},
doi = {10.3390/microorganisms9010148},
pmid = {33440837},
issn = {2076-2607},
support = {BiodivUP//State-Region Planning Contracts (CPER), European Regional Development Fund (FEDER)/ ; },
abstract = {The crucial role of microbes in the evolution, development, health, and ecological interactions of multicellular organisms is now widely recognized in the holobiont concept. However, the structure and stability of microbiota are highly dependent on abiotic and biotic factors, especially in the gut, which can be colonized by transient bacteria depending on the host's diet. We studied these impacts by manipulating the digestive microbiota of the detritivore Armadillidium vulgare and analyzing the consequences on its structure and function. Hosts were exposed to initial starvation and then were fed diets that varied the different components of lignocellulose. A total of 72 digestive microbiota were analyzed according to the type of the diet (standard or enriched in cellulose, lignin, or hemicellulose) and the period following dysbiosis. The results showed that microbiota from the hepatopancreas were very stable and resilient, while the most diverse and labile over time were found in the hindgut. Dysbiosis and selective diets may have affected the host fitness by altering the structure of the microbiota and its predicted functions. Overall, these modifications can therefore have effects not only on the holobiont, but also on the "eco-holobiont" conceptualization of macroorganisms.},
}
RevDate: 2021-01-13
Viral speciation through subcellular genetic isolation and virogenesis incompatibility.
Nature communications, 12(1):342.
Understanding how biological species arise is critical for understanding the evolution of life on Earth. Bioinformatic analyses have recently revealed that viruses, like multicellular life, form reproductively isolated biological species. Viruses are known to share high rates of genetic exchange, so how do they evolve genetic isolation? Here, we evaluate two related bacteriophages and describe three factors that limit genetic exchange between them: 1) A nucleus-like compartment that physically separates replicating phage genomes, thereby limiting inter-phage recombination during co-infection; 2) A tubulin-based spindle that orchestrates phage replication and forms nonfunctional hybrid polymers; and 3) A nuclear incompatibility factor that reduces phage fitness. Together, these traits maintain species differences through Subcellular Genetic Isolation where viral genomes are physically separated during co-infection, and Virogenesis Incompatibility in which the interaction of cross-species components interferes with viral production.
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@article {pmid33436625,
year = {2021},
author = {Chaikeeratisak, V and Birkholz, EA and Prichard, AM and Egan, ME and Mylvara, A and Nonejuie, P and Nguyen, KT and Sugie, J and Meyer, JR and Pogliano, J},
title = {Viral speciation through subcellular genetic isolation and virogenesis incompatibility.},
journal = {Nature communications},
volume = {12},
number = {1},
pages = {342},
pmid = {33436625},
issn = {2041-1723},
abstract = {Understanding how biological species arise is critical for understanding the evolution of life on Earth. Bioinformatic analyses have recently revealed that viruses, like multicellular life, form reproductively isolated biological species. Viruses are known to share high rates of genetic exchange, so how do they evolve genetic isolation? Here, we evaluate two related bacteriophages and describe three factors that limit genetic exchange between them: 1) A nucleus-like compartment that physically separates replicating phage genomes, thereby limiting inter-phage recombination during co-infection; 2) A tubulin-based spindle that orchestrates phage replication and forms nonfunctional hybrid polymers; and 3) A nuclear incompatibility factor that reduces phage fitness. Together, these traits maintain species differences through Subcellular Genetic Isolation where viral genomes are physically separated during co-infection, and Virogenesis Incompatibility in which the interaction of cross-species components interferes with viral production.},
}
RevDate: 2021-01-08
Expanding ecological assessment by integrating microorganisms into routine freshwater biomonitoring.
Water research, 191:116767 pii:S0043-1354(20)31300-2 [Epub ahead of print].
Bioindication has become an indispensable part of water quality monitoring in most countries of the world, with the presence and abundance of bioindicator taxa, mostly multicellular eukaryotes, used for biotic indices. In contrast, microbes (bacteria, archaea and protists) are seldom used as bioindicators in routine assessments, although they have been recognized for their importance in environmental processes. Recently, the use of molecular methods has revealed unexpected diversity within known functional groups and novel metabolic pathways that are particularly important in energy and nutrient cycling. In various habitats, microbial communities respond to eutrophication, metals, and natural or anthropogenic organic pollutants through changes in diversity and function. In this review, we evaluated the common trends in these changes, documenting that they have value as bioindicators and can be used not only for monitoring but also for improving our understanding of the major processes in lotic and lentic environments. Current knowledge provides a solid foundation for exploiting microbial taxa, community structures and diversity, as well as functional genes, in novel monitoring programs. These microbial community measures can also be combined into biotic indices, improving the resolution of individual bioindicators. Here, we assess particular molecular approaches complemented by advanced bioinformatic analysis, as these are the most promising with respect to detailed bioindication value. We conclude that microbial community dynamics are a missing link important for our understanding of rapid changes in the structure and function of aquatic ecosystems, and should be addressed in the future environmental monitoring of freshwater ecosystems.
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@article {pmid33418487,
year = {2020},
author = {Sagova-Mareckova, M and Boenigk, J and Bouchez, A and Cermakova, K and Chonova, T and Cordier, T and Eisendle, U and Elersek, T and Fazi, S and Fleituch, T and Frühe, L and Gajdosova, M and Graupner, N and Haegerbaeumer, A and Kelly, AM and Kopecky, J and Leese, F and Nõges, P and Orlic, S and Panksep, K and Pawlowski, J and Petrusek, A and Piggott, JJ and Rusch, JC and Salis, R and Schenk, J and Simek, K and Stovicek, A and Strand, DA and Vasquez, MI and Vrålstad, T and Zlatkovic, S and Zupancic, M and Stoeck, T},
title = {Expanding ecological assessment by integrating microorganisms into routine freshwater biomonitoring.},
journal = {Water research},
volume = {191},
number = {},
pages = {116767},
doi = {10.1016/j.watres.2020.116767},
pmid = {33418487},
issn = {1879-2448},
abstract = {Bioindication has become an indispensable part of water quality monitoring in most countries of the world, with the presence and abundance of bioindicator taxa, mostly multicellular eukaryotes, used for biotic indices. In contrast, microbes (bacteria, archaea and protists) are seldom used as bioindicators in routine assessments, although they have been recognized for their importance in environmental processes. Recently, the use of molecular methods has revealed unexpected diversity within known functional groups and novel metabolic pathways that are particularly important in energy and nutrient cycling. In various habitats, microbial communities respond to eutrophication, metals, and natural or anthropogenic organic pollutants through changes in diversity and function. In this review, we evaluated the common trends in these changes, documenting that they have value as bioindicators and can be used not only for monitoring but also for improving our understanding of the major processes in lotic and lentic environments. Current knowledge provides a solid foundation for exploiting microbial taxa, community structures and diversity, as well as functional genes, in novel monitoring programs. These microbial community measures can also be combined into biotic indices, improving the resolution of individual bioindicators. Here, we assess particular molecular approaches complemented by advanced bioinformatic analysis, as these are the most promising with respect to detailed bioindication value. We conclude that microbial community dynamics are a missing link important for our understanding of rapid changes in the structure and function of aquatic ecosystems, and should be addressed in the future environmental monitoring of freshwater ecosystems.},
}
RevDate: 2021-01-07
Introduction to the Theme "Old and New Toxicology: Interfaces with Pharmacology".
Annual review of pharmacology and toxicology, 61:1-7.
The theme of Volume 61 is "Old and New Toxicology: Interfaces with Pharmacology." Old toxicology is exemplified by the authors of the autobiographical articles: B.M. Olivera's work on toxins and venoms from cone snails and P. Taylor's studies of acetylcholinesterase and the nicotinic cholinergic receptor, which serve as sites of action for numerous pesticides and venoms. Other articles in this volume focus on new understanding and new types of toxicology, including (a) arsenic toxicity, which is an ancient poison that, through evolution, has caused most multicellular organisms to express an active arsenic methyltransferase to methylate arsenite, which accelerates the excretion of arsenic from the body; (b) small molecules that react with lipid dicarbonyls, which are now considered the most toxic oxidative stress end products; (c) immune checkpoint inhibitors (ICIs), which have revolutionized cancer therapy but have numerous immune-related adverse events, including cardiovascular complications; (d) autoimmunity caused by the environment; (e) idiosyncratic drug-induced liver disease, which together with the toxicity of ICIs represents new toxicology interfacing with pharmacology; and (f) sex differences in the development of cardiovascular disease, with men more susceptible than women to vascular inflammation that initiates and perpetuates disease. These articles and others in Volume 61 reflect the interface and close integration of pharmacology and toxicology that began long ago but continues today.
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@article {pmid33411582,
year = {2021},
author = {Costa, M and Blaschke, TF and Amara, SG and Meyer, UA and Insel, PA},
title = {Introduction to the Theme "Old and New Toxicology: Interfaces with Pharmacology".},
journal = {Annual review of pharmacology and toxicology},
volume = {61},
number = {},
pages = {1-7},
doi = {10.1146/annurev-pharmtox-092220-033032},
pmid = {33411582},
issn = {1545-4304},
abstract = {The theme of Volume 61 is "Old and New Toxicology: Interfaces with Pharmacology." Old toxicology is exemplified by the authors of the autobiographical articles: B.M. Olivera's work on toxins and venoms from cone snails and P. Taylor's studies of acetylcholinesterase and the nicotinic cholinergic receptor, which serve as sites of action for numerous pesticides and venoms. Other articles in this volume focus on new understanding and new types of toxicology, including (a) arsenic toxicity, which is an ancient poison that, through evolution, has caused most multicellular organisms to express an active arsenic methyltransferase to methylate arsenite, which accelerates the excretion of arsenic from the body; (b) small molecules that react with lipid dicarbonyls, which are now considered the most toxic oxidative stress end products; (c) immune checkpoint inhibitors (ICIs), which have revolutionized cancer therapy but have numerous immune-related adverse events, including cardiovascular complications; (d) autoimmunity caused by the environment; (e) idiosyncratic drug-induced liver disease, which together with the toxicity of ICIs represents new toxicology interfacing with pharmacology; and (f) sex differences in the development of cardiovascular disease, with men more susceptible than women to vascular inflammation that initiates and perpetuates disease. These articles and others in Volume 61 reflect the interface and close integration of pharmacology and toxicology that began long ago but continues today.},
}
RevDate: 2021-01-03
Insight into early diversification of leucine-rich repeat receptor-like kinases provided by the sequenced moss and hornwort genomes.
Plant molecular biology [Epub ahead of print].
KEY MESSAGE: Identification of the subfamily X leucine-rich repeat receptor-like kinases in the recently sequenced moss and hornwort genomes points to their diversification into distinct groups during early evolution of land plants. Signal transduction mediated through receptor-ligand interactions plays key roles in controlling developmental and physiological processes of multicellular organisms, and plants employ diverse receptors in signaling. Leucine-rich repeat receptor-like kinases (LRR-RLKs) represent one of the largest receptor classes in plants and are structurally classified into subfamilies. LRR-RLKs of the subfamily X are unique in the variety of their signaling roles; they include receptors for steroid or peptide hormones as well as negative regulators of signaling through binding to other LRR-RLKs, raising a question as to how they diversified. However, our understanding of diversification processes of LRR-RLKs has been hindered by the paucity of genomic data in non-seed plants and limited taxa sampling in previous phylogenetic analyses. Here we analyzed the phylogeny of LRR-RLK X sequences collected from all major land plant lineages and show that this subfamily diversified into six major clades before the divergence between bryophytes and vascular plants. Notably, we have identified homologues of the brassinosteroid receptor, BRASSINOSTEROID INSENSITIVE 1 (BRI1), in the genomes of Sphagnum mosses, hornworts, and ferns, contrary to earlier reports that postulate the origin of BRI1-like LRR-RLKs in the seed plant lineage. The phylogenetic distribution of major clades illustrates that the current receptor repertoire was shaped through lineage-specific gene family expansion and independent gene losses, highlighting dynamic changes in the evolution of LRR-RLKs.
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@article {pmid33389562,
year = {2021},
author = {Furumizu, C and Sawa, S},
title = {Insight into early diversification of leucine-rich repeat receptor-like kinases provided by the sequenced moss and hornwort genomes.},
journal = {Plant molecular biology},
volume = {},
number = {},
pages = {},
pmid = {33389562},
issn = {1573-5028},
support = {17H03967//Japan Society for the Promotion of Science/ ; 18H04841//Japan Society for the Promotion of Science/ ; 18H04625//Japan Society for the Promotion of Science/ ; 18H05487//Japan Society for the Promotion of Science/ ; 20H00422//Japan Society for the Promotion of Science/ ; 20K06770//Japan Society for the Promotion of Science/ ; },
abstract = {KEY MESSAGE: Identification of the subfamily X leucine-rich repeat receptor-like kinases in the recently sequenced moss and hornwort genomes points to their diversification into distinct groups during early evolution of land plants. Signal transduction mediated through receptor-ligand interactions plays key roles in controlling developmental and physiological processes of multicellular organisms, and plants employ diverse receptors in signaling. Leucine-rich repeat receptor-like kinases (LRR-RLKs) represent one of the largest receptor classes in plants and are structurally classified into subfamilies. LRR-RLKs of the subfamily X are unique in the variety of their signaling roles; they include receptors for steroid or peptide hormones as well as negative regulators of signaling through binding to other LRR-RLKs, raising a question as to how they diversified. However, our understanding of diversification processes of LRR-RLKs has been hindered by the paucity of genomic data in non-seed plants and limited taxa sampling in previous phylogenetic analyses. Here we analyzed the phylogeny of LRR-RLK X sequences collected from all major land plant lineages and show that this subfamily diversified into six major clades before the divergence between bryophytes and vascular plants. Notably, we have identified homologues of the brassinosteroid receptor, BRASSINOSTEROID INSENSITIVE 1 (BRI1), in the genomes of Sphagnum mosses, hornworts, and ferns, contrary to earlier reports that postulate the origin of BRI1-like LRR-RLKs in the seed plant lineage. The phylogenetic distribution of major clades illustrates that the current receptor repertoire was shaped through lineage-specific gene family expansion and independent gene losses, highlighting dynamic changes in the evolution of LRR-RLKs.},
}
RevDate: 2020-12-29
Evolution of Adrenoleukodystrophy Model Systems.
Journal of inherited metabolic disease [Epub ahead of print].
X-linked adrenoleukodystrophy (ALD) is a neurometabolic disorder affecting the adrenal glands, testes, spinal cord and brain. The disease is caused by mutations in the ABCD1 gene resulting in a defect in peroxisomal degradation of very long-chain fatty acids (VLCFA) and their accumulation in plasma and tissues. Males with ALD have a near 100% life-time risk to develop myelopathy. The life-time prevelance to develop progressive cerebral white matter lesions (known as cerebral ALD) is about 60%. Adrenal insufficiency occurs in about 80% of male patients. In adulthood, 80% of women with ALD also develop myelopathy, but adrenal insufficiency or cerebral ALD are very rare. The complex clinical presentation and the absence of a genotype-phenotype correlation are complicating our understanding of the disease. In an attempt to understand the pathophysiology of ALD various model systems have been developed. While these model systems share the basic genetics and biochemistry of ALD they fail to fully recapitulate the complex neurodegenerative etiology of ALD. Each model system recapitulates certain aspects of the disorder. This exposes the complexity of ALD and therefore the challenge to create a comprehensive model system to fully understand ALD. In this review, we provide an overview of the different ALD modelling strategies from single-celled to multicellular organisms and from in vitro to in vivo approaches, and introduce how emerging iPSC-derived technologies could improve the understanding of this highly complex disorder. This article is protected by copyright. All rights reserved.
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@article {pmid33373044,
year = {2020},
author = {Montoro, R and Heine, VM and Kemp, S and Engelen, M},
title = {Evolution of Adrenoleukodystrophy Model Systems.},
journal = {Journal of inherited metabolic disease},
volume = {},
number = {},
pages = {},
doi = {10.1002/jimd.12357},
pmid = {33373044},
issn = {1573-2665},
abstract = {X-linked adrenoleukodystrophy (ALD) is a neurometabolic disorder affecting the adrenal glands, testes, spinal cord and brain. The disease is caused by mutations in the ABCD1 gene resulting in a defect in peroxisomal degradation of very long-chain fatty acids (VLCFA) and their accumulation in plasma and tissues. Males with ALD have a near 100% life-time risk to develop myelopathy. The life-time prevelance to develop progressive cerebral white matter lesions (known as cerebral ALD) is about 60%. Adrenal insufficiency occurs in about 80% of male patients. In adulthood, 80% of women with ALD also develop myelopathy, but adrenal insufficiency or cerebral ALD are very rare. The complex clinical presentation and the absence of a genotype-phenotype correlation are complicating our understanding of the disease. In an attempt to understand the pathophysiology of ALD various model systems have been developed. While these model systems share the basic genetics and biochemistry of ALD they fail to fully recapitulate the complex neurodegenerative etiology of ALD. Each model system recapitulates certain aspects of the disorder. This exposes the complexity of ALD and therefore the challenge to create a comprehensive model system to fully understand ALD. In this review, we provide an overview of the different ALD modelling strategies from single-celled to multicellular organisms and from in vitro to in vivo approaches, and introduce how emerging iPSC-derived technologies could improve the understanding of this highly complex disorder. This article is protected by copyright. All rights reserved.},
}
RevDate: 2020-12-23
Stem Cells for Next Level Toxicity Testing in the 21st Century.
Small (Weinheim an der Bergstrasse, Germany) [Epub ahead of print].
The call for a paradigm change in toxicology from the United States National Research Council in 2007 initiates awareness for the invention and use of human-relevant alternative methods for toxicological hazard assessment. Simple 2D in vitro systems may serve as first screening tools, however, recent developments infer the need for more complex, multicellular organotypic models, which are superior in mimicking the complexity of human organs. In this review article most critical organs for toxicity assessment, i.e., skin, brain, thyroid system, lung, heart, liver, kidney, and intestine are discussed with regards to their functions in health and disease. Embracing the manifold modes-of-action how xenobiotic compounds can interfere with physiological organ functions and cause toxicity, the need for translation of such multifaceted organ features into the dish seems obvious. Currently used in vitro methods for toxicological applications and ongoing developments not yet arrived in toxicity testing are discussed, especially highlighting the potential of models based on embryonic stem cells and induced pluripotent stem cells of human origin. Finally, the application of innovative technologies like organs-on-a-chip and genome editing point toward a toxicological paradigm change moves into action.
Additional Links: PMID-33354870
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@article {pmid33354870,
year = {2020},
author = {Fritsche, E and Haarmann-Stemmann, T and Kapr, J and Galanjuk, S and Hartmann, J and Mertens, PR and Kämpfer, AAM and Schins, RPF and Tigges, J and Koch, K},
title = {Stem Cells for Next Level Toxicity Testing in the 21st Century.},
journal = {Small (Weinheim an der Bergstrasse, Germany)},
volume = {},
number = {},
pages = {e2006252},
doi = {10.1002/smll.202006252},
pmid = {33354870},
issn = {1613-6829},
support = {233-1.08.03.03-121972/131//State of North-Rhine Westphalia, Germany/ ; 1.08.03.03//State of North-Rhine Westphalia, Germany/ ; 121972//State of North-Rhine Westphalia, Germany/ ; //European Union's Horizon 2020 Research and Innovation Program/ ; 825759//Grant Agreement/ ; 97850925//German Research Foundation/ ; SFB 854//German Research Foundation/ ; GRK 2408//German Research Foundation/ ; ME-1365/7-2//German Research Foundation/ ; ME-1365/9-2//German Research Foundation/ ; 825759//Horizon 2020/ ; },
abstract = {The call for a paradigm change in toxicology from the United States National Research Council in 2007 initiates awareness for the invention and use of human-relevant alternative methods for toxicological hazard assessment. Simple 2D in vitro systems may serve as first screening tools, however, recent developments infer the need for more complex, multicellular organotypic models, which are superior in mimicking the complexity of human organs. In this review article most critical organs for toxicity assessment, i.e., skin, brain, thyroid system, lung, heart, liver, kidney, and intestine are discussed with regards to their functions in health and disease. Embracing the manifold modes-of-action how xenobiotic compounds can interfere with physiological organ functions and cause toxicity, the need for translation of such multifaceted organ features into the dish seems obvious. Currently used in vitro methods for toxicological applications and ongoing developments not yet arrived in toxicity testing are discussed, especially highlighting the potential of models based on embryonic stem cells and induced pluripotent stem cells of human origin. Finally, the application of innovative technologies like organs-on-a-chip and genome editing point toward a toxicological paradigm change moves into action.},
}
RevDate: 2020-12-17
Stepping From Modeling Cancer Plasticity to the Philosophy of Cancer.
Frontiers in genetics, 11:579738.
Additional Links: PMID-33329717
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@article {pmid33329717,
year = {2020},
author = {Clairambault, J},
title = {Stepping From Modeling Cancer Plasticity to the Philosophy of Cancer.},
journal = {Frontiers in genetics},
volume = {11},
number = {},
pages = {579738},
doi = {10.3389/fgene.2020.579738},
pmid = {33329717},
issn = {1664-8021},
}
RevDate: 2020-12-17
Nanovirus Disease Complexes: An Emerging Threat in the Modern Era.
Frontiers in plant science, 11:558403.
Multipartite viruses package their genomic segments independently and mainly infect plants; few target animals. Nanoviridae is a family of multipartite single-stranded DNA plant viruses that individually encapsidate single-stranded DNAs of approximately 1 kb and transmit them through aphids without replication in the aphid vectors, thereby causing important diseases of leguminous crops and banana. Significant findings regarding nanoviruses have recently been made on important features, such as their multicellular way of life, the transmission of distinct encapsidated genome segments through the vector body, evolutionary ambiguities, mode of infection, host range and geographical distribution. This review deals with all the above-mentioned features in view of recent advances with special emphasis on the emergence of new species and recognition of new host range of nanoviruses and aims to shed light on the evolutionary linkages, the potentially devastating impact on the world economy, and the future challenges imposed by nanoviruses.
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@article {pmid33329624,
year = {2020},
author = {Lal, A and Vo, TTB and Sanjaya, IGNPW and Ho, PT and Kim, JK and Kil, EJ and Lee, S},
title = {Nanovirus Disease Complexes: An Emerging Threat in the Modern Era.},
journal = {Frontiers in plant science},
volume = {11},
number = {},
pages = {558403},
doi = {10.3389/fpls.2020.558403},
pmid = {33329624},
issn = {1664-462X},
abstract = {Multipartite viruses package their genomic segments independently and mainly infect plants; few target animals. Nanoviridae is a family of multipartite single-stranded DNA plant viruses that individually encapsidate single-stranded DNAs of approximately 1 kb and transmit them through aphids without replication in the aphid vectors, thereby causing important diseases of leguminous crops and banana. Significant findings regarding nanoviruses have recently been made on important features, such as their multicellular way of life, the transmission of distinct encapsidated genome segments through the vector body, evolutionary ambiguities, mode of infection, host range and geographical distribution. This review deals with all the above-mentioned features in view of recent advances with special emphasis on the emergence of new species and recognition of new host range of nanoviruses and aims to shed light on the evolutionary linkages, the potentially devastating impact on the world economy, and the future challenges imposed by nanoviruses.},
}
RevDate: 2020-12-14
CmpDate: 2020-12-04
OsChz1 acts as a histone chaperone in modulating chromatin organization and genome function in rice.
Nature communications, 11(1):5717.
While the yeast Chz1 acts as a specific histone-chaperone for H2A.Z, functions of CHZ-domain proteins in multicellular eukaryotes remain obscure. Here, we report on the functional characterization of OsChz1, a sole CHZ-domain protein identified in rice. OsChz1 interacts with both the canonical H2A-H2B dimer and the variant H2A.Z-H2B dimer. Within crystal structure the C-terminal region of OsChz1 binds H2A-H2B via an acidic region, pointing to a previously unknown recognition mechanism. Knockout of OsChz1 leads to multiple plant developmental defects. At genome-wide level, loss of OsChz1 causes mis-regulations of thousands of genes and broad alterations of nucleosome occupancy as well as reductions of H2A.Z-enrichment. While OsChz1 associates with chromatin regions enriched of repressive histone marks (H3K27me3 and H3K4me2), its loss does not affect the genome landscape of DNA methylation. Taken together, it is emerging that OsChz1 functions as an important H2A/H2A.Z-H2B chaperone in dynamic regulation of chromatin for higher eukaryote development.
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@article {pmid33177521,
year = {2020},
author = {Du, K and Luo, Q and Yin, L and Wu, J and Liu, Y and Gan, J and Dong, A and Shen, WH},
title = {OsChz1 acts as a histone chaperone in modulating chromatin organization and genome function in rice.},
journal = {Nature communications},
volume = {11},
number = {1},
pages = {5717},
pmid = {33177521},
issn = {2041-1723},
mesh = {CRISPR-Cas Systems ; Chromatin/genetics/*metabolism ; DNA Methylation ; Flowers/metabolism ; Gene Expression Regulation, Plant ; Genome, Plant ; Histones/genetics/*metabolism ; Molecular Chaperones/genetics/metabolism ; Mutation ; Nucleosomes/genetics ; Oryza/*genetics/growth & development/metabolism ; Phylogeny ; Plant Proteins/genetics/*metabolism ; Plants, Genetically Modified ; Protein Multimerization ; },
abstract = {While the yeast Chz1 acts as a specific histone-chaperone for H2A.Z, functions of CHZ-domain proteins in multicellular eukaryotes remain obscure. Here, we report on the functional characterization of OsChz1, a sole CHZ-domain protein identified in rice. OsChz1 interacts with both the canonical H2A-H2B dimer and the variant H2A.Z-H2B dimer. Within crystal structure the C-terminal region of OsChz1 binds H2A-H2B via an acidic region, pointing to a previously unknown recognition mechanism. Knockout of OsChz1 leads to multiple plant developmental defects. At genome-wide level, loss of OsChz1 causes mis-regulations of thousands of genes and broad alterations of nucleosome occupancy as well as reductions of H2A.Z-enrichment. While OsChz1 associates with chromatin regions enriched of repressive histone marks (H3K27me3 and H3K4me2), its loss does not affect the genome landscape of DNA methylation. Taken together, it is emerging that OsChz1 functions as an important H2A/H2A.Z-H2B chaperone in dynamic regulation of chromatin for higher eukaryote development.},
}
MeSH Terms:
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hide MeSH Terms
CRISPR-Cas Systems
Chromatin/genetics/*metabolism
DNA Methylation
Flowers/metabolism
Gene Expression Regulation, Plant
Genome, Plant
Histones/genetics/*metabolism
Molecular Chaperones/genetics/metabolism
Mutation
Nucleosomes/genetics
Oryza/*genetics/growth & development/metabolism
Phylogeny
Plant Proteins/genetics/*metabolism
Plants, Genetically Modified
Protein Multimerization
RevDate: 2020-12-14
CmpDate: 2020-12-04
Multicellular growth of the Basidiomycota phytopathogen fungus Sporisorium reilianum induced by acid conditions.
Folia microbiologica, 65(3):511-521.
Fungi are considered model organisms for the analysis of important phenomena of eukaryotes. For example, some of them have been described as models to understand the phenomenon of multicellularity acquisition by different unicellular organisms phylogenetically distant. Interestingly, in this work, we describe the multicellular development in the model fungus S. reilianum. We observed that Sporisorium reilianum, a Basidiomycota cereal pathogen that at neutral pH grows with a yeast-like morphology during its saprophytic haploid stage, when incubated at acid pH grew in the form of multicellular clusters. The multicellularity observed in S. reilianum was of clonal type, where buds of "stem" cells growing as yeasts remain joined by their cell wall septa, after cytokinesis. The elaboration and analysis of a regulatory network of S. reilianum showed that the putative zinc finger transcription factor CBQ73544.1 regulates a number of genes involved in cell cycle, cellular division, signal transduction pathways, and biogenesis of cell wall. Interestingly, homologous of these genes have been found to be regulated during Saccharomyces cerevisiae multicellular growth. In adddition, some of these genes were found to be negatively regulated during multicellularity of S. reilianum. With these data, we suggest that S. reilianum is an interesting model for the study of multicellular development.
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@article {pmid31721091,
year = {2020},
author = {Martínez-Soto, D and Velez-Haro, JM and León-Ramírez, CG and Galán-Vásquez, E and Chávez-Munguía, B and Ruiz-Herrera, J},
title = {Multicellular growth of the Basidiomycota phytopathogen fungus Sporisorium reilianum induced by acid conditions.},
journal = {Folia microbiologica},
volume = {65},
number = {3},
pages = {511-521},
doi = {10.1007/s12223-019-00755-7},
pmid = {31721091},
issn = {1874-9356},
mesh = {Acids/*pharmacology ; Basidiomycota/drug effects/*genetics/*growth & development ; Cell Cycle/drug effects ; Cell Division/drug effects ; Fungal Proteins/*genetics ; Hydrogen-Ion Concentration ; Phylogeny ; Signal Transduction/drug effects ; },
abstract = {Fungi are considered model organisms for the analysis of important phenomena of eukaryotes. For example, some of them have been described as models to understand the phenomenon of multicellularity acquisition by different unicellular organisms phylogenetically distant. Interestingly, in this work, we describe the multicellular development in the model fungus S. reilianum. We observed that Sporisorium reilianum, a Basidiomycota cereal pathogen that at neutral pH grows with a yeast-like morphology during its saprophytic haploid stage, when incubated at acid pH grew in the form of multicellular clusters. The multicellularity observed in S. reilianum was of clonal type, where buds of "stem" cells growing as yeasts remain joined by their cell wall septa, after cytokinesis. The elaboration and analysis of a regulatory network of S. reilianum showed that the putative zinc finger transcription factor CBQ73544.1 regulates a number of genes involved in cell cycle, cellular division, signal transduction pathways, and biogenesis of cell wall. Interestingly, homologous of these genes have been found to be regulated during Saccharomyces cerevisiae multicellular growth. In adddition, some of these genes were found to be negatively regulated during multicellularity of S. reilianum. With these data, we suggest that S. reilianum is an interesting model for the study of multicellular development.},
}
MeSH Terms:
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Acids/*pharmacology
Basidiomycota/drug effects/*genetics/*growth & development
Cell Cycle/drug effects
Cell Division/drug effects
Fungal Proteins/*genetics
Hydrogen-Ion Concentration
Phylogeny
Signal Transduction/drug effects
RevDate: 2020-12-14
CmpDate: 2020-12-08
Do cells use passwords in cell-state transitions? Is cell signaling sometimes encrypted?.
Theory in biosciences = Theorie in den Biowissenschaften, 139(1):87-93.
Organisms must maintain proper regulation including defense and healing. Life-threatening problems may be caused by pathogens or by a multicellular organism's own cells through cancer or autoimmune disorders. Life evolved solutions to these problems that can be conceptualized through the lens of information security, which is a well-developed field in computer science. Here I argue that taking an information security view of cells is not merely semantics, but useful to explain features of signaling, regulation, and defense. An information security perspective also offers a conduit for cross-fertilization of advanced ideas from computer science and the potential for biology to inform computer science. First, I consider whether cells use passwords, i.e., initiation sequences that are required for subsequent signals to have effects, by analyzing the concept of pioneer transcription factors in chromatin regulation and cellular reprogramming. Second, I consider whether cells may encrypt signal transduction cascades. Encryption could benefit cells by making it more difficult for pathogens or oncogenes to hijack cell networks. By using numerous molecules, cells may gain a security advantage in particular against viruses, whose genome sizes are typically under selection pressure. I provide a simple conceptual argument for how cells may perform encryption through posttranslational modifications, complex formation, and chromatin accessibility. I invoke information theory to provide a criterion of an entropy spike to assess whether a signaling cascade has encryption-like features. I discuss how the frequently invoked concept of context dependency may oversimplify more advanced features of cell signaling networks, such as encryption. Therefore, by considering that biochemical networks may be even more complex than commonly realized we may be better able to understand defenses against pathogens and pathologies.
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@article {pmid31175621,
year = {2020},
author = {Root, A},
title = {Do cells use passwords in cell-state transitions? Is cell signaling sometimes encrypted?.},
journal = {Theory in biosciences = Theorie in den Biowissenschaften},
volume = {139},
number = {1},
pages = {87-93},
pmid = {31175621},
issn = {1611-7530},
mesh = {Algorithms ; Animals ; Autoimmune Diseases/*metabolism ; Biological Evolution ; Biological Phenomena ; Chromatin/metabolism ; Computational Biology ; Entropy ; Environment ; Genome ; Humans ; Immune System ; *Models, Biological ; Neoplasms/*metabolism ; Neurons/metabolism ; Semantics ; *Signal Transduction ; },
abstract = {Organisms must maintain proper regulation including defense and healing. Life-threatening problems may be caused by pathogens or by a multicellular organism's own cells through cancer or autoimmune disorders. Life evolved solutions to these problems that can be conceptualized through the lens of information security, which is a well-developed field in computer science. Here I argue that taking an information security view of cells is not merely semantics, but useful to explain features of signaling, regulation, and defense. An information security perspective also offers a conduit for cross-fertilization of advanced ideas from computer science and the potential for biology to inform computer science. First, I consider whether cells use passwords, i.e., initiation sequences that are required for subsequent signals to have effects, by analyzing the concept of pioneer transcription factors in chromatin regulation and cellular reprogramming. Second, I consider whether cells may encrypt signal transduction cascades. Encryption could benefit cells by making it more difficult for pathogens or oncogenes to hijack cell networks. By using numerous molecules, cells may gain a security advantage in particular against viruses, whose genome sizes are typically under selection pressure. I provide a simple conceptual argument for how cells may perform encryption through posttranslational modifications, complex formation, and chromatin accessibility. I invoke information theory to provide a criterion of an entropy spike to assess whether a signaling cascade has encryption-like features. I discuss how the frequently invoked concept of context dependency may oversimplify more advanced features of cell signaling networks, such as encryption. Therefore, by considering that biochemical networks may be even more complex than commonly realized we may be better able to understand defenses against pathogens and pathologies.},
}
MeSH Terms:
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Algorithms
Animals
Autoimmune Diseases/*metabolism
Biological Evolution
Biological Phenomena
Chromatin/metabolism
Computational Biology
Entropy
Environment
Genome
Humans
Immune System
*Models, Biological
Neoplasms/*metabolism
Neurons/metabolism
Semantics
*Signal Transduction
RevDate: 2020-12-11
P53 induces senescence in the unstable progeny of aneuploid cells.
Cell cycle (Georgetown, Tex.) [Epub ahead of print].
Aneuploidy is the condition of having an imbalanced karyotype, which is associated with tumor initiation, evolution, and acquisition of drug-resistant features, possibly by generating heterogeneous populations of cells with distinct genotypes and phenotypes. Multicellular eukaryotes have therefore evolved a range of extrinsic and cell-autonomous mechanisms for restraining proliferation of aneuploid cells, including activation of the tumor suppressor protein p53. However, accumulating evidence indicates that a subset of aneuploid cells can escape p53-mediated growth restriction and continue proliferating in vitro. Here we show that such aneuploid cell lines display a robust modal karyotype and low frequency of chromosomal aberrations despite ongoing chromosome instability. Indeed, while these aneuploid cells are able to survive for extended periods in vitro, their chromosomally unstable progeny remain subject to p53-induced senescence and growth restriction, leading to subsequent elimination from the aneuploid pool. This mechanism helps maintain low levels of heterogeneity in aneuploid populations and may prevent detrimental evolutionary processes such as cancer progression and development of drug resistance.
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@article {pmid33305692,
year = {2020},
author = {Giam, M and Wong, CK and Low, JS and Sinelli, M and Dreesen, O and Rancati, G},
title = {P53 induces senescence in the unstable progeny of aneuploid cells.},
journal = {Cell cycle (Georgetown, Tex.)},
volume = {},
number = {},
pages = {1-13},
doi = {10.1080/15384101.2020.1850968},
pmid = {33305692},
issn = {1551-4005},
abstract = {Aneuploidy is the condition of having an imbalanced karyotype, which is associated with tumor initiation, evolution, and acquisition of drug-resistant features, possibly by generating heterogeneous populations of cells with distinct genotypes and phenotypes. Multicellular eukaryotes have therefore evolved a range of extrinsic and cell-autonomous mechanisms for restraining proliferation of aneuploid cells, including activation of the tumor suppressor protein p53. However, accumulating evidence indicates that a subset of aneuploid cells can escape p53-mediated growth restriction and continue proliferating in vitro. Here we show that such aneuploid cell lines display a robust modal karyotype and low frequency of chromosomal aberrations despite ongoing chromosome instability. Indeed, while these aneuploid cells are able to survive for extended periods in vitro, their chromosomally unstable progeny remain subject to p53-induced senescence and growth restriction, leading to subsequent elimination from the aneuploid pool. This mechanism helps maintain low levels of heterogeneity in aneuploid populations and may prevent detrimental evolutionary processes such as cancer progression and development of drug resistance.},
}
RevDate: 2020-12-09
Identifying cancer-associated fibroblasts as emerging targets for hepatocellular carcinoma.
Cell & bioscience, 10(1):127 pii:10.1186/s13578-020-00488-y.
The tumor microenvironment (TME) is a complex multicellular functional compartment that includes fibroblasts, myofibroblasts, endothelial cells, immune cells, and extracellular matrix (ECM) elements. The microenvironment provides an optimum condition for the initiation, growth, and dissemination of hepatocellular carcinoma (HCC). As one of the critical and abundant components in tumor microenvironment, cancer-associated fibroblasts (CAFs) have been implicated in the progression of HCC. Through secreting various growth factors and cytokines, CAFs contribute to the ECM remodeling, stem features, angiogenesis, immunosuppression, and vasculogenic mimicry (VM), which reinforce the initiation and development of HCC. In order to restrain the CAFs-initiated HCC progression, current strategies include targeting specific markers, engineering CAFs with tumor-suppressive phenotype, depleting CAFs' precursors, and repressing the secretions or downstream signaling. In this review, we update the emerging understanding of CAFs in HCC, with particular emphasis on cellular origin, phenotypes, biological functions and targeted strategies. It provides insights into the targeting CAFs for HCC treatment.
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@article {pmid33292459,
year = {2020},
author = {Zhang, J and Gu, C and Song, Q and Zhu, M and Xu, Y and Xiao, M and Zheng, W},
title = {Identifying cancer-associated fibroblasts as emerging targets for hepatocellular carcinoma.},
journal = {Cell & bioscience},
volume = {10},
number = {1},
pages = {127},
doi = {10.1186/s13578-020-00488-y},
pmid = {33292459},
issn = {2045-3701},
support = {81702419//National Natural Science Foundation of China/ ; BE2019692//Key Research and Development Program of Jiangxi Province/ ; MS12019013//Nantong Science and Technology Bureau/ ; MS22018006//Nantong Science and Technology Bureau/ ; },
abstract = {The tumor microenvironment (TME) is a complex multicellular functional compartment that includes fibroblasts, myofibroblasts, endothelial cells, immune cells, and extracellular matrix (ECM) elements. The microenvironment provides an optimum condition for the initiation, growth, and dissemination of hepatocellular carcinoma (HCC). As one of the critical and abundant components in tumor microenvironment, cancer-associated fibroblasts (CAFs) have been implicated in the progression of HCC. Through secreting various growth factors and cytokines, CAFs contribute to the ECM remodeling, stem features, angiogenesis, immunosuppression, and vasculogenic mimicry (VM), which reinforce the initiation and development of HCC. In order to restrain the CAFs-initiated HCC progression, current strategies include targeting specific markers, engineering CAFs with tumor-suppressive phenotype, depleting CAFs' precursors, and repressing the secretions or downstream signaling. In this review, we update the emerging understanding of CAFs in HCC, with particular emphasis on cellular origin, phenotypes, biological functions and targeted strategies. It provides insights into the targeting CAFs for HCC treatment.},
}
RevDate: 2020-12-04
Towards understanding the origin of animal development.
Development (Cambridge, England), 147(23): pii:147/23/dev192575.
Almost all animals undergo embryonic development, going from a single-celled zygote to a complex multicellular adult. We know that the patterning and morphogenetic processes involved in development are deeply conserved within the animal kingdom. However, the origins of these developmental processes are just beginning to be unveiled. Here, we focus on how the protist lineages sister to animals are reshaping our view of animal development. Most intriguingly, many of these protistan lineages display transient multicellular structures, which are governed by similar morphogenetic and gene regulatory processes as animal development. We discuss here two potential alternative scenarios to explain the origin of animal embryonic development: either it originated concomitantly at the onset of animals or it evolved from morphogenetic processes already present in their unicellular ancestors. We propose that an integrative study of several unicellular taxa closely related to animals will allow a more refined picture of how the last common ancestor of animals underwent embryonic development.
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@article {pmid33272929,
year = {2020},
author = {Ruiz-Trillo, I and de Mendoza, A},
title = {Towards understanding the origin of animal development.},
journal = {Development (Cambridge, England)},
volume = {147},
number = {23},
pages = {},
doi = {10.1242/dev.192575},
pmid = {33272929},
issn = {1477-9129},
abstract = {Almost all animals undergo embryonic development, going from a single-celled zygote to a complex multicellular adult. We know that the patterning and morphogenetic processes involved in development are deeply conserved within the animal kingdom. However, the origins of these developmental processes are just beginning to be unveiled. Here, we focus on how the protist lineages sister to animals are reshaping our view of animal development. Most intriguingly, many of these protistan lineages display transient multicellular structures, which are governed by similar morphogenetic and gene regulatory processes as animal development. We discuss here two potential alternative scenarios to explain the origin of animal embryonic development: either it originated concomitantly at the onset of animals or it evolved from morphogenetic processes already present in their unicellular ancestors. We propose that an integrative study of several unicellular taxa closely related to animals will allow a more refined picture of how the last common ancestor of animals underwent embryonic development.},
}
RevDate: 2020-12-03
Comparative Analysis of ROS Network Genes in Extremophile Eukaryotes.
International journal of molecular sciences, 21(23): pii:ijms21239131.
The reactive oxygen species (ROS) gene network, consisting of both ROS-generating and detoxifying enzymes, adjusts ROS levels in response to various stimuli. We performed a cross-kingdom comparison of ROS gene networks to investigate how they have evolved across all Eukaryotes, including protists, fungi, plants and animals. We included the genomes of 16 extremotolerant Eukaryotes to gain insight into ROS gene evolution in organisms that experience extreme stress conditions. Our analysis focused on ROS genes found in all Eukaryotes (such as catalases, superoxide dismutases, glutathione reductases, peroxidases and glutathione peroxidase/peroxiredoxins) as well as those specific to certain groups, such as ascorbate peroxidases, dehydroascorbate/monodehydroascorbate reductases in plants and other photosynthetic organisms. ROS-producing NADPH oxidases (NOX) were found in most multicellular organisms, although several NOX-like genes were identified in unicellular or filamentous species. However, despite the extreme conditions experienced by extremophile species, we found no evidence for expansion of ROS-related gene families in these species compared to other Eukaryotes. Tardigrades and rotifers do show ROS gene expansions that could be related to their extreme lifestyles, although a high rate of lineage-specific horizontal gene transfer events, coupled with recent tetraploidy in rotifers, could explain this observation. This suggests that the basal Eukaryotic ROS scavenging systems are sufficient to maintain ROS homeostasis even under the most extreme conditions.
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@article {pmid33266251,
year = {2020},
author = {Lyall, R and Nikoloski, Z and Gechev, T},
title = {Comparative Analysis of ROS Network Genes in Extremophile Eukaryotes.},
journal = {International journal of molecular sciences},
volume = {21},
number = {23},
pages = {},
doi = {10.3390/ijms21239131},
pmid = {33266251},
issn = {1422-0067},
support = {SGA-CSA No. 739582//Project PlantaSYST, European Union's Horizon 2020 Research & Innovation Programme/ ; GA No. 823746//Project RESIST, European Union's Horizon 2020 Research & Innovation Programme/ ; BG05M2OP001-1.003-001-C01//European Regional Development Fund/ ; },
abstract = {The reactive oxygen species (ROS) gene network, consisting of both ROS-generating and detoxifying enzymes, adjusts ROS levels in response to various stimuli. We performed a cross-kingdom comparison of ROS gene networks to investigate how they have evolved across all Eukaryotes, including protists, fungi, plants and animals. We included the genomes of 16 extremotolerant Eukaryotes to gain insight into ROS gene evolution in organisms that experience extreme stress conditions. Our analysis focused on ROS genes found in all Eukaryotes (such as catalases, superoxide dismutases, glutathione reductases, peroxidases and glutathione peroxidase/peroxiredoxins) as well as those specific to certain groups, such as ascorbate peroxidases, dehydroascorbate/monodehydroascorbate reductases in plants and other photosynthetic organisms. ROS-producing NADPH oxidases (NOX) were found in most multicellular organisms, although several NOX-like genes were identified in unicellular or filamentous species. However, despite the extreme conditions experienced by extremophile species, we found no evidence for expansion of ROS-related gene families in these species compared to other Eukaryotes. Tardigrades and rotifers do show ROS gene expansions that could be related to their extreme lifestyles, although a high rate of lineage-specific horizontal gene transfer events, coupled with recent tetraploidy in rotifers, could explain this observation. This suggests that the basal Eukaryotic ROS scavenging systems are sufficient to maintain ROS homeostasis even under the most extreme conditions.},
}
RevDate: 2020-12-02
Symbiotic Origin of Apoptosis.
Results and problems in cell differentiation, 69:253-280.
The progress of evolutionary biology has revealed that symbiosis played a basic role in the evolution of complex eukaryotic organisms, including humans. Mitochondria are actually simplified endosymbiotic bacteria currently playing the role of cellular organelles. Mitochondrial domestication occurred at the very beginning of eukaryotic evolution. Mitochondria have two different basic functions: they produce energy using oxidative respiration, and they initiate different forms of apoptotic programmed/regulated cell death. Apoptotic programmed cell death may have different cytological forms. Mechanisms of apoptotic programmed cell death exist even in the unicellular organisms, and they play a basic role in the development of complex multicellular organisms, such as fungi, green plants, and animals. Multicellularity was independently established many times among eukaryotes. There are indications that apoptotic programmed cell death is a trait required for the establishment of multicellularity. Regulated cell death is initiated by many different parallel biochemical pathways. It is generally accepted that apoptosis evolved during mitochondrial domestication. However, there are different hypothetical models of the origin of apoptosis. The phylogenetic studies of my group indicate that apoptosis probably evolved during an evolutionary arms race between host ancestral eukaryotic predators and ancestral prey mitochondria (named protomitochondria). Protomitochondrial prey produced many different toxins as a defense against predators. From these toxins evolved extant apoptotic factors. There are indications that aerobic respiration and apoptosis co-evolved and are functionally linked in extant organisms. Perturbations of apoptosis and oxidative respiration are frequently observed during neoplastic transition. Our group showed that perturbations of apoptosis in yeasts also cause perturbations of oxidative respiration.
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@article {pmid33263876,
year = {2020},
author = {Kaczanowski, S},
title = {Symbiotic Origin of Apoptosis.},
journal = {Results and problems in cell differentiation},
volume = {69},
number = {},
pages = {253-280},
doi = {10.1007/978-3-030-51849-3_10},
pmid = {33263876},
issn = {0080-1844},
abstract = {The progress of evolutionary biology has revealed that symbiosis played a basic role in the evolution of complex eukaryotic organisms, including humans. Mitochondria are actually simplified endosymbiotic bacteria currently playing the role of cellular organelles. Mitochondrial domestication occurred at the very beginning of eukaryotic evolution. Mitochondria have two different basic functions: they produce energy using oxidative respiration, and they initiate different forms of apoptotic programmed/regulated cell death. Apoptotic programmed cell death may have different cytological forms. Mechanisms of apoptotic programmed cell death exist even in the unicellular organisms, and they play a basic role in the development of complex multicellular organisms, such as fungi, green plants, and animals. Multicellularity was independently established many times among eukaryotes. There are indications that apoptotic programmed cell death is a trait required for the establishment of multicellularity. Regulated cell death is initiated by many different parallel biochemical pathways. It is generally accepted that apoptosis evolved during mitochondrial domestication. However, there are different hypothetical models of the origin of apoptosis. The phylogenetic studies of my group indicate that apoptosis probably evolved during an evolutionary arms race between host ancestral eukaryotic predators and ancestral prey mitochondria (named protomitochondria). Protomitochondrial prey produced many different toxins as a defense against predators. From these toxins evolved extant apoptotic factors. There are indications that aerobic respiration and apoptosis co-evolved and are functionally linked in extant organisms. Perturbations of apoptosis and oxidative respiration are frequently observed during neoplastic transition. Our group showed that perturbations of apoptosis in yeasts also cause perturbations of oxidative respiration.},
}
RevDate: 2020-12-02
Gap junctions amplify spatial variations in cell volume in proliferating tumor spheroids.
Nature communications, 11(1):6148 pii:10.1038/s41467-020-19904-5.
Sustained proliferation is a significant driver of cancer progression. Cell-cycle advancement is coupled with cell size, but it remains unclear how multiple cells interact to control their volume in 3D clusters. In this study, we propose a mechano-osmotic model to investigate the evolution of volume dynamics within multicellular systems. Volume control depends on an interplay between multiple cellular constituents, including gap junctions, mechanosensitive ion channels, energy-consuming ion pumps, and the actomyosin cortex, that coordinate to manipulate cellular osmolarity. In connected cells, we show that mechanical loading leads to the emergence of osmotic pressure gradients between cells with consequent increases in cellular ion concentrations driving swelling. We identify how gap junctions can amplify spatial variations in cell volume within multicellular spheroids and, further, describe how the process depends on proliferation-induced solid stress. Our model may provide new insight into the role of gap junctions in breast cancer progression.
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@article {pmid33262337,
year = {2020},
author = {McEvoy, E and Han, YL and Guo, M and Shenoy, VB},
title = {Gap junctions amplify spatial variations in cell volume in proliferating tumor spheroids.},
journal = {Nature communications},
volume = {11},
number = {1},
pages = {6148},
doi = {10.1038/s41467-020-19904-5},
pmid = {33262337},
issn = {2041-1723},
support = {U01 CA202177/CA/NCI NIH HHS/United States ; U54 CA193417/CA/NCI NIH HHS/United States ; R01 CA232256/CA/NCI NIH HHS/United States ; U01 CA202123/CA/NCI NIH HHS/United States ; R01 EB017753/EB/NIBIB NIH HHS/United States ; R01 EB030876/EB/NIBIB NIH HHS/United States ; },
abstract = {Sustained proliferation is a significant driver of cancer progression. Cell-cycle advancement is coupled with cell size, but it remains unclear how multiple cells interact to control their volume in 3D clusters. In this study, we propose a mechano-osmotic model to investigate the evolution of volume dynamics within multicellular systems. Volume control depends on an interplay between multiple cellular constituents, including gap junctions, mechanosensitive ion channels, energy-consuming ion pumps, and the actomyosin cortex, that coordinate to manipulate cellular osmolarity. In connected cells, we show that mechanical loading leads to the emergence of osmotic pressure gradients between cells with consequent increases in cellular ion concentrations driving swelling. We identify how gap junctions can amplify spatial variations in cell volume within multicellular spheroids and, further, describe how the process depends on proliferation-induced solid stress. Our model may provide new insight into the role of gap junctions in breast cancer progression.},
}
RevDate: 2020-12-01
The genetic basis for the evolution of soma: mechanistic evidence for the co-option of a stress-induced gene into a developmental master regulator.
Proceedings. Biological sciences, 287(1940):20201414.
In multicellular organisms with specialized cells, the most significant distinction among cell types is between reproductive (germ) cells and non-reproductive/somatic cells (soma). Although soma contributed to the marked increase in complexity of many multicellular lineages, little is known about its evolutionary origins. We have previously suggested that the evolution of genes responsible for the differentiation of somatic cells involved the co-option of life history trade-off genes that in unicellular organisms enhanced survival at a cost to immediate reproduction. In the multicellular green alga, Volvox carteri, cell fate is established early in development by the differential expression of a master regulatory gene known as regA. A closely related RegA-Like Sequence (RLS1) is present in its single-celled relative, Chlamydomonas reinhardtii. RLS1 is expressed in response to stress, and we proposed that an environmentally induced RLS1-like gene was co-opted into a developmental pathway in the lineage leading to V. carteri. However, the exact evolutionary scenario responsible for the postulated co-option event remains to be determined. Here, we show that in addition to being developmentally regulated, regA can also be induced by environmental cues, indicating that regA has maintained its ancestral regulation. We also found that the absence of a functional RegA protein confers increased sensitivity to stress, consistent with RegA having a direct or indirect role in stress responses. Overall, this study (i) provides mechanistic evidence for the co-option of an environmentally induced gene into a major developmental regulator, (ii) supports the view that major morphological innovations can evolve via regulatory changes and (iii) argues for the role of stress in the evolution of multicellular complexity.
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@article {pmid33259762,
year = {2020},
author = {König, SG and Nedelcu, AM},
title = {The genetic basis for the evolution of soma: mechanistic evidence for the co-option of a stress-induced gene into a developmental master regulator.},
journal = {Proceedings. Biological sciences},
volume = {287},
number = {1940},
pages = {20201414},
doi = {10.1098/rspb.2020.1414},
pmid = {33259762},
issn = {1471-2954},
abstract = {In multicellular organisms with specialized cells, the most significant distinction among cell types is between reproductive (germ) cells and non-reproductive/somatic cells (soma). Although soma contributed to the marked increase in complexity of many multicellular lineages, little is known about its evolutionary origins. We have previously suggested that the evolution of genes responsible for the differentiation of somatic cells involved the co-option of life history trade-off genes that in unicellular organisms enhanced survival at a cost to immediate reproduction. In the multicellular green alga, Volvox carteri, cell fate is established early in development by the differential expression of a master regulatory gene known as regA. A closely related RegA-Like Sequence (RLS1) is present in its single-celled relative, Chlamydomonas reinhardtii. RLS1 is expressed in response to stress, and we proposed that an environmentally induced RLS1-like gene was co-opted into a developmental pathway in the lineage leading to V. carteri. However, the exact evolutionary scenario responsible for the postulated co-option event remains to be determined. Here, we show that in addition to being developmentally regulated, regA can also be induced by environmental cues, indicating that regA has maintained its ancestral regulation. We also found that the absence of a functional RegA protein confers increased sensitivity to stress, consistent with RegA having a direct or indirect role in stress responses. Overall, this study (i) provides mechanistic evidence for the co-option of an environmentally induced gene into a major developmental regulator, (ii) supports the view that major morphological innovations can evolve via regulatory changes and (iii) argues for the role of stress in the evolution of multicellular complexity.},
}
RevDate: 2020-12-01
Mites, ticks, anaphylaxis and allergy: The Acari hypothesis.
Medical hypotheses, 144:110257.
Anaphylaxis is a poorly understood immune process in which a Th2-/IgE-mediated adaptive response commandeers cellular machinery, typically reserved for defense against multicellular ectoparasites, to activate against otherwise benign molecules. Its clinical manifestations consist of rapid pathophysiological reflexes that target epithelial surfaces. The galactose-α-1,3-galactose hypersensitivity response is a compelling model of anaphylaxis for which causation has been demonstrated. At the core of the model, a tick bite sensitizes a recipient to a tick foodstuff. As proposed herein, the model likely informs on the origin of all allergic inflammation; namely, allergy is not intended to protect against seemingly harmless and irrelevant materials, but is, instead, intended to rid epithelial surfaces of pathogen-bearing Acari, i.e., mites and ticks. The demonstrated adjuvant activity of acarian gastrointestinal secretions, when paired with the polyphagous diet of mites, renders acarians eminently suited to accounting, mechanistically, for many, if not all, human allergies.
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@article {pmid33254563,
year = {2020},
author = {Retzinger, AC and Retzinger, GS},
title = {Mites, ticks, anaphylaxis and allergy: The Acari hypothesis.},
journal = {Medical hypotheses},
volume = {144},
number = {},
pages = {110257},
doi = {10.1016/j.mehy.2020.110257},
pmid = {33254563},
issn = {1532-2777},
abstract = {Anaphylaxis is a poorly understood immune process in which a Th2-/IgE-mediated adaptive response commandeers cellular machinery, typically reserved for defense against multicellular ectoparasites, to activate against otherwise benign molecules. Its clinical manifestations consist of rapid pathophysiological reflexes that target epithelial surfaces. The galactose-α-1,3-galactose hypersensitivity response is a compelling model of anaphylaxis for which causation has been demonstrated. At the core of the model, a tick bite sensitizes a recipient to a tick foodstuff. As proposed herein, the model likely informs on the origin of all allergic inflammation; namely, allergy is not intended to protect against seemingly harmless and irrelevant materials, but is, instead, intended to rid epithelial surfaces of pathogen-bearing Acari, i.e., mites and ticks. The demonstrated adjuvant activity of acarian gastrointestinal secretions, when paired with the polyphagous diet of mites, renders acarians eminently suited to accounting, mechanistically, for many, if not all, human allergies.},
}
RevDate: 2020-11-28
Transcriptomic and Proteomic Analysis of Mannitol-metabolism-associated Genes in Saccharina japonica.
Genomics, proteomics & bioinformatics pii:S1672-0229(20)30130-3 [Epub ahead of print].
As a carbon-storage compound and osmoprotectant in brown algae, mannitol is synthesized and then accumulated at high levels in Saccharina japonica (Sja); however, the underlying control mechanisms have not been studied. Our analysis of genomic and transcriptomic data from Sja shows that mannitol metabolism is a cyclic pathway composed of four distinct steps. A mannitol-1-phosphate dehydrogenase (M1PDH2) and two mannitol-1-phosphatases (M1Pase) work together or in combination to exhibit full enzymatic properties. Based on comprehensive transcriptomic data from different tissues, generations, and sexes as well as under different stress conditions, coupled with droplet digital PCR (ddPCR) and proteomic confirmation, we suggest that SjaM1Pase1 plays a major role in mannitol biosynthesis and that the basic mannitol anabolism and the carbohydrate pool dynamics are responsible for carbon storage and anti-stress mechanism. Our proteomic data indicate that mannitol metabolism remains constant during diurnal cycle in Sja. In addition, we discover that mannitol-metabolism-associated (MMA) genes show differential expression between the multicellular filamentous (gametophyte) and large parenchymal thallus (sporophyte) generations and respond differentially to environmental stresses, such as hyposaline and hyperthermic conditions. Our results indicate that the ecophysiological significance of such differentially expressed genes may be attributable to the evolution of heteromorphic generations (filamentous and thallus) and environmental adaptation of Laminariales.
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@article {pmid33248278,
year = {2020},
author = {Chi, S and Wang, G and Liu, T and Wang, X and Liu, C and Jin, Y and Yin, H and Xu, X and Yu, J},
title = {Transcriptomic and Proteomic Analysis of Mannitol-metabolism-associated Genes in Saccharina japonica.},
journal = {Genomics, proteomics & bioinformatics},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.gpb.2018.12.012},
pmid = {33248278},
issn = {2210-3244},
abstract = {As a carbon-storage compound and osmoprotectant in brown algae, mannitol is synthesized and then accumulated at high levels in Saccharina japonica (Sja); however, the underlying control mechanisms have not been studied. Our analysis of genomic and transcriptomic data from Sja shows that mannitol metabolism is a cyclic pathway composed of four distinct steps. A mannitol-1-phosphate dehydrogenase (M1PDH2) and two mannitol-1-phosphatases (M1Pase) work together or in combination to exhibit full enzymatic properties. Based on comprehensive transcriptomic data from different tissues, generations, and sexes as well as under different stress conditions, coupled with droplet digital PCR (ddPCR) and proteomic confirmation, we suggest that SjaM1Pase1 plays a major role in mannitol biosynthesis and that the basic mannitol anabolism and the carbohydrate pool dynamics are responsible for carbon storage and anti-stress mechanism. Our proteomic data indicate that mannitol metabolism remains constant during diurnal cycle in Sja. In addition, we discover that mannitol-metabolism-associated (MMA) genes show differential expression between the multicellular filamentous (gametophyte) and large parenchymal thallus (sporophyte) generations and respond differentially to environmental stresses, such as hyposaline and hyperthermic conditions. Our results indicate that the ecophysiological significance of such differentially expressed genes may be attributable to the evolution of heteromorphic generations (filamentous and thallus) and environmental adaptation of Laminariales.},
}
RevDate: 2020-11-27
Ecological and Evolutionary Consequences of Anticancer Adaptations.
iScience, 23(11):101716.
Cellular cheating leading to cancers exists in all branches of multicellular life, favoring the evolution of adaptations to avoid or suppress malignant progression, and/or to alleviate its fitness consequences. Ecologists have until recently largely neglected the importance of cancer cells for animal ecology, presumably because they did not consider either the potential ecological or evolutionary consequences of anticancer adaptations. Here, we review the diverse ways in which the evolution of anticancer adaptations has significantly constrained several aspects of the evolutionary ecology of multicellular organisms at the cell, individual, population, species, and ecosystem levels and suggest some avenues for future research.
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@article {pmid33241195,
year = {2020},
author = {Boutry, J and Dujon, AM and Gerard, AL and Tissot, S and Macdonald, N and Schultz, A and Biro, PA and Beckmann, C and Hamede, R and Hamilton, DG and Giraudeau, M and Ujvari, B and Thomas, F},
title = {Ecological and Evolutionary Consequences of Anticancer Adaptations.},
journal = {iScience},
volume = {23},
number = {11},
pages = {101716},
pmid = {33241195},
issn = {2589-0042},
abstract = {Cellular cheating leading to cancers exists in all branches of multicellular life, favoring the evolution of adaptations to avoid or suppress malignant progression, and/or to alleviate its fitness consequences. Ecologists have until recently largely neglected the importance of cancer cells for animal ecology, presumably because they did not consider either the potential ecological or evolutionary consequences of anticancer adaptations. Here, we review the diverse ways in which the evolution of anticancer adaptations has significantly constrained several aspects of the evolutionary ecology of multicellular organisms at the cell, individual, population, species, and ecosystem levels and suggest some avenues for future research.},
}
RevDate: 2020-11-29
Photosynthetic hydrogen production by droplet-based microbial micro-reactors under aerobic conditions.
Nature communications, 11(1):5985 pii:10.1038/s41467-020-19823-5.
The spontaneous self-assembly of multicellular ensembles into living materials with synergistic structure and function remains a considerable challenge in biotechnology and synthetic biology. Here, we exploit the aqueous two-phase separation of dextran-in-PEG emulsion micro-droplets for the capture, spatial organization and immobilization of algal cells or algal/bacterial cell communities to produce discrete multicellular spheroids capable of both aerobic (oxygen producing) and hypoxic (hydrogen producing) photosynthesis in daylight under air. We show that localized oxygen depletion results in hydrogen production from the core of the algal microscale reactor, and demonstrate that enhanced levels of hydrogen evolution can be achieved synergistically by spontaneously enclosing the photosynthetic cells within a shell of bacterial cells undergoing aerobic respiration. Our results highlight a promising droplet-based environmentally benign approach to dispersible photosynthetic microbial micro-reactors comprising segregated cellular micro-niches with dual functionality, and provide a step towards photobiological hydrogen production under aerobic conditions.
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@article {pmid33239636,
year = {2020},
author = {Xu, Z and Wang, S and Zhao, C and Li, S and Liu, X and Wang, L and Li, M and Huang, X and Mann, S},
title = {Photosynthetic hydrogen production by droplet-based microbial micro-reactors under aerobic conditions.},
journal = {Nature communications},
volume = {11},
number = {1},
pages = {5985},
doi = {10.1038/s41467-020-19823-5},
pmid = {33239636},
issn = {2041-1723},
abstract = {The spontaneous self-assembly of multicellular ensembles into living materials with synergistic structure and function remains a considerable challenge in biotechnology and synthetic biology. Here, we exploit the aqueous two-phase separation of dextran-in-PEG emulsion micro-droplets for the capture, spatial organization and immobilization of algal cells or algal/bacterial cell communities to produce discrete multicellular spheroids capable of both aerobic (oxygen producing) and hypoxic (hydrogen producing) photosynthesis in daylight under air. We show that localized oxygen depletion results in hydrogen production from the core of the algal microscale reactor, and demonstrate that enhanced levels of hydrogen evolution can be achieved synergistically by spontaneously enclosing the photosynthetic cells within a shell of bacterial cells undergoing aerobic respiration. Our results highlight a promising droplet-based environmentally benign approach to dispersible photosynthetic microbial micro-reactors comprising segregated cellular micro-niches with dual functionality, and provide a step towards photobiological hydrogen production under aerobic conditions.},
}
RevDate: 2020-11-24
The order of trait emergence in the evolution of cyanobacterial multicellularity.
Genome biology and evolution pii:5999801 [Epub ahead of print].
The transition from unicellular to multicellular organisms is one of the most significant events in the history of life. Key to this process is the emergence of Darwinian individuality at the higher level: groups must become single entities capable of reproduction for selection to shape their evolution. Evolutionary transitions in individuality are characterized by cooperation between the lower level entities and by division of labor. Theory suggests that division of labor may drive the transition to multicellularity by eliminating the trade-off between two incompatible processes that cannot be performed simultaneously in one cell. Here we examine the evolution of the most ancient multicellular transition known today, that of cyanobacteria, where we reconstruct the sequence of ecological and phenotypic trait evolution. Our results show that the prime driver of multicellularity in cyanobacteria was the expansion in metabolic capacity offered by nitrogen fixation, which was accompanied by the emergence of the filamentous morphology and succeeded by a reproductive life cycle. This was followed by the progression of multicellularity into higher complexity in the form of differentiated cells and patterned multicellularity.
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@article {pmid33231627,
year = {2020},
author = {Hammerschmidt, K and Landan, G and Tria, FDK and Alcorta, J and Dagan, T},
title = {The order of trait emergence in the evolution of cyanobacterial multicellularity.},
journal = {Genome biology and evolution},
volume = {},
number = {},
pages = {},
doi = {10.1093/gbe/evaa249},
pmid = {33231627},
issn = {1759-6653},
abstract = {The transition from unicellular to multicellular organisms is one of the most significant events in the history of life. Key to this process is the emergence of Darwinian individuality at the higher level: groups must become single entities capable of reproduction for selection to shape their evolution. Evolutionary transitions in individuality are characterized by cooperation between the lower level entities and by division of labor. Theory suggests that division of labor may drive the transition to multicellularity by eliminating the trade-off between two incompatible processes that cannot be performed simultaneously in one cell. Here we examine the evolution of the most ancient multicellular transition known today, that of cyanobacteria, where we reconstruct the sequence of ecological and phenotypic trait evolution. Our results show that the prime driver of multicellularity in cyanobacteria was the expansion in metabolic capacity offered by nitrogen fixation, which was accompanied by the emergence of the filamentous morphology and succeeded by a reproductive life cycle. This was followed by the progression of multicellularity into higher complexity in the form of differentiated cells and patterned multicellularity.},
}
RevDate: 2020-11-24
Brown Algal Model Organisms.
Annual review of genetics, 54:71-92.
Model organisms are extensively used in research as accessible and convenient systems for studying a particular area or question in biology. Traditionally, only a limited number of organisms have been studied in detail, but modern genomic tools are enabling researchers to extend beyond the set of classical model organisms to include novel species from less-studied phylogenetic groups. This review focuses on model species for an important group of multicellular organisms, the brown algae. The development of genetic and genomic tools for the filamentous brown alga Ectocarpus has led to it emerging as a general model system for this group, but additional models, such as Fucus or Dictyota dichotoma, remain of interest for specific biological questions. In addition, Saccharina japonica has emerged as a model system to directly address applied questions related to algal aquaculture. We discuss the past, present, and future of brown algal model organisms in relation to the opportunities and challenges in brown algal research.
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@article {pmid33228413,
year = {2020},
author = {Coelho, SM and Cock, JM},
title = {Brown Algal Model Organisms.},
journal = {Annual review of genetics},
volume = {54},
number = {},
pages = {71-92},
doi = {10.1146/annurev-genet-030620-093031},
pmid = {33228413},
issn = {1545-2948},
abstract = {Model organisms are extensively used in research as accessible and convenient systems for studying a particular area or question in biology. Traditionally, only a limited number of organisms have been studied in detail, but modern genomic tools are enabling researchers to extend beyond the set of classical model organisms to include novel species from less-studied phylogenetic groups. This review focuses on model species for an important group of multicellular organisms, the brown algae. The development of genetic and genomic tools for the filamentous brown alga Ectocarpus has led to it emerging as a general model system for this group, but additional models, such as Fucus or Dictyota dichotoma, remain of interest for specific biological questions. In addition, Saccharina japonica has emerged as a model system to directly address applied questions related to algal aquaculture. We discuss the past, present, and future of brown algal model organisms in relation to the opportunities and challenges in brown algal research.},
}
RevDate: 2020-12-01
Phylostratic Shift of Whole-Genome Duplications in Normal Mammalian Tissues towards Unicellularity Is Driven by Developmental Bivalent Genes and Reveals a Link to Cancer.
International journal of molecular sciences, 21(22):.
Tumours were recently revealed to undergo a phylostratic and phenotypic shift to unicellularity. As well, aggressive tumours are characterized by an increased proportion of polyploid cells. In order to investigate a possible shared causation of these two features, we performed a comparative phylostratigraphic analysis of ploidy-related genes, obtained from transcriptomic data for polyploid and diploid human and mouse tissues using pairwise cross-species transcriptome comparison and principal component analysis. Our results indicate that polyploidy shifts the evolutionary age balance of the expressed genes from the late metazoan phylostrata towards the upregulation of unicellular and early metazoan phylostrata. The up-regulation of unicellular metabolic and drug-resistance pathways and the downregulation of pathways related to circadian clock were identified. This evolutionary shift was associated with the enrichment of ploidy with bivalent genes (p < 10-16). The protein interactome of activated bivalent genes revealed the increase of the connectivity of unicellulars and (early) multicellulars, while circadian regulators were depressed. The mutual polyploidy-c-MYC-bivalent genes-associated protein network was organized by gene-hubs engaged in both embryonic development and metastatic cancer including driver (proto)-oncogenes of viral origin. Our data suggest that, in cancer, the atavistic shift goes hand-in-hand with polyploidy and is driven by epigenetic mechanisms impinging on development-related bivalent genes.
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@article {pmid33228223,
year = {2020},
author = {Anatskaya, OV and Vinogradov, AE and Vainshelbaum, NM and Giuliani, A and Erenpreisa, J},
title = {Phylostratic Shift of Whole-Genome Duplications in Normal Mammalian Tissues towards Unicellularity Is Driven by Developmental Bivalent Genes and Reveals a Link to Cancer.},
journal = {International journal of molecular sciences},
volume = {21},
number = {22},
pages = {},
pmid = {33228223},
issn = {1422-0067},
support = {1.1.1.1/18/A/099//European Regional Development Fund (ERDF)/ ; 12//Institute of Cytology Director's Fund/ ; XX//Natural Sciences PhD Student Scholarship from the University of Latvia Foundation/ ; },
abstract = {Tumours were recently revealed to undergo a phylostratic and phenotypic shift to unicellularity. As well, aggressive tumours are characterized by an increased proportion of polyploid cells. In order to investigate a possible shared causation of these two features, we performed a comparative phylostratigraphic analysis of ploidy-related genes, obtained from transcriptomic data for polyploid and diploid human and mouse tissues using pairwise cross-species transcriptome comparison and principal component analysis. Our results indicate that polyploidy shifts the evolutionary age balance of the expressed genes from the late metazoan phylostrata towards the upregulation of unicellular and early metazoan phylostrata. The up-regulation of unicellular metabolic and drug-resistance pathways and the downregulation of pathways related to circadian clock were identified. This evolutionary shift was associated with the enrichment of ploidy with bivalent genes (p < 10-16). The protein interactome of activated bivalent genes revealed the increase of the connectivity of unicellulars and (early) multicellulars, while circadian regulators were depressed. The mutual polyploidy-c-MYC-bivalent genes-associated protein network was organized by gene-hubs engaged in both embryonic development and metastatic cancer including driver (proto)-oncogenes of viral origin. Our data suggest that, in cancer, the atavistic shift goes hand-in-hand with polyploidy and is driven by epigenetic mechanisms impinging on development-related bivalent genes.},
}
RevDate: 2020-11-20
The Timing of Evolutionary Transitions Suggests Intelligent Life Is Rare.
Astrobiology [Epub ahead of print].
It is unknown how abundant extraterrestrial life is, or whether such life might be complex or intelligent. On Earth, the emergence of complex intelligent life required a preceding series of evolutionary transitions such as abiogenesis, eukaryogenesis, and the evolution of sexual reproduction, multicellularity, and intelligence itself. Some of these transitions could have been extraordinarily improbable, even in conducive environments. The emergence of intelligent life late in Earth's lifetime is thought to be evidence for a handful of rare evolutionary transitions, but the timing of other evolutionary transitions in the fossil record is yet to be analyzed in a similar framework. Using a simplified Bayesian model that combines uninformative priors and the timing of evolutionary transitions, we demonstrate that expected evolutionary transition times likely exceed the lifetime of Earth, perhaps by many orders of magnitude. Our results corroborate the original argument suggested by Brandon Carter that intelligent life in the Universe is exceptionally rare, assuming that intelligent life elsewhere requires analogous evolutionary transitions. Arriving at the opposite conclusion would require exceptionally conservative priors, evidence for much earlier transitions, multiple instances of transitions, or an alternative model that can explain why evolutionary transitions took hundreds of millions of years without appealing to rare chance events. Although the model is simple, it provides an initial basis for evaluating how varying biological assumptions and fossil record data impact the probability of evolving intelligent life, and also provides a number of testable predictions, such as that some biological paradoxes will remain unresolved and that planets orbiting M dwarf stars are uninhabitable.
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@article {pmid33216655,
year = {2020},
author = {Snyder-Beattie, AE and Sandberg, A and Drexler, KE and Bonsall, MB},
title = {The Timing of Evolutionary Transitions Suggests Intelligent Life Is Rare.},
journal = {Astrobiology},
volume = {},
number = {},
pages = {},
doi = {10.1089/ast.2019.2149},
pmid = {33216655},
issn = {1557-8070},
abstract = {It is unknown how abundant extraterrestrial life is, or whether such life might be complex or intelligent. On Earth, the emergence of complex intelligent life required a preceding series of evolutionary transitions such as abiogenesis, eukaryogenesis, and the evolution of sexual reproduction, multicellularity, and intelligence itself. Some of these transitions could have been extraordinarily improbable, even in conducive environments. The emergence of intelligent life late in Earth's lifetime is thought to be evidence for a handful of rare evolutionary transitions, but the timing of other evolutionary transitions in the fossil record is yet to be analyzed in a similar framework. Using a simplified Bayesian model that combines uninformative priors and the timing of evolutionary transitions, we demonstrate that expected evolutionary transition times likely exceed the lifetime of Earth, perhaps by many orders of magnitude. Our results corroborate the original argument suggested by Brandon Carter that intelligent life in the Universe is exceptionally rare, assuming that intelligent life elsewhere requires analogous evolutionary transitions. Arriving at the opposite conclusion would require exceptionally conservative priors, evidence for much earlier transitions, multiple instances of transitions, or an alternative model that can explain why evolutionary transitions took hundreds of millions of years without appealing to rare chance events. Although the model is simple, it provides an initial basis for evaluating how varying biological assumptions and fossil record data impact the probability of evolving intelligent life, and also provides a number of testable predictions, such as that some biological paradoxes will remain unresolved and that planets orbiting M dwarf stars are uninhabitable.},
}
RevDate: 2020-11-19
Evolution of multicellular life cycles under costly fragmentation.
PLoS computational biology, 16(11):e1008406 pii:PCOMPBIOL-D-20-00157 [Epub ahead of print].
A fascinating wealth of life cycles is observed in biology, from unicellularity to the concerted fragmentation of multicellular units. However, the understanding of factors driving their evolution is still limited. We show that costs of fragmentation have a major impact on the evolution of life cycles due to their influence on the growth rates of the associated populations. We model a group structured population of undifferentiated cells, where cell clusters reproduce by fragmentation. Fragmentation events are associated with a cost expressed by either a fragmentation delay, an additional risk, or a cell loss. The introduction of such fragmentation costs vastly increases the set of possible life cycles. Based on these findings, we suggest that the evolution of life cycles involving splitting into multiple offspring can be directly associated with the fragmentation cost. Moreover, the impact of this cost alone is strong enough to drive the emergence of multicellular units that eventually split into many single cells, even under scenarios that strongly disfavour collectives compared to solitary individuals.
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@article {pmid33211685,
year = {2020},
author = {Pichugin, Y and Traulsen, A},
title = {Evolution of multicellular life cycles under costly fragmentation.},
journal = {PLoS computational biology},
volume = {16},
number = {11},
pages = {e1008406},
doi = {10.1371/journal.pcbi.1008406},
pmid = {33211685},
issn = {1553-7358},
abstract = {A fascinating wealth of life cycles is observed in biology, from unicellularity to the concerted fragmentation of multicellular units. However, the understanding of factors driving their evolution is still limited. We show that costs of fragmentation have a major impact on the evolution of life cycles due to their influence on the growth rates of the associated populations. We model a group structured population of undifferentiated cells, where cell clusters reproduce by fragmentation. Fragmentation events are associated with a cost expressed by either a fragmentation delay, an additional risk, or a cell loss. The introduction of such fragmentation costs vastly increases the set of possible life cycles. Based on these findings, we suggest that the evolution of life cycles involving splitting into multiple offspring can be directly associated with the fragmentation cost. Moreover, the impact of this cost alone is strong enough to drive the emergence of multicellular units that eventually split into many single cells, even under scenarios that strongly disfavour collectives compared to solitary individuals.},
}
RevDate: 2020-11-19
Transmissible cancers and the evolution of sex under the Red Queen hypothesis.
PLoS biology, 18(11):e3000916 pii:PBIOLOGY-D-20-00851.
The predominance of sexual reproduction in eukaryotes remains paradoxical in evolutionary theory. Of the hypotheses proposed to resolve this paradox, the 'Red Queen hypothesis' emphasises the potential of antagonistic interactions to cause fluctuating selection, which favours the evolution and maintenance of sex. Whereas empirical and theoretical developments have focused on host-parasite interactions, the premises of the Red Queen theory apply equally well to any type of antagonistic interactions. Recently, it has been suggested that early multicellular organisms with basic anticancer defences were presumably plagued by antagonistic interactions with transmissible cancers and that this could have played a pivotal role in the evolution of sex. Here, we dissect this argument using a population genetic model. One fundamental aspect distinguishing transmissible cancers from other parasites is the continual production of cancerous cell lines from hosts' own tissues. We show that this influx dampens fluctuating selection and therefore makes the evolution of sex more difficult than in standard Red Queen models. Although coevolutionary cycling can remain sufficient to select for sex under some parameter regions of our model, we show that the size of those regions shrinks once we account for epidemiological constraints. Altogether, our results suggest that horizontal transmission of cancerous cells is unlikely to cause fluctuating selection favouring sexual reproduction. Nonetheless, we confirm that vertical transmission of cancerous cells can promote the evolution of sex through a separate mechanism, known as similarity selection, that does not depend on coevolutionary fluctuations.
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@article {pmid33211684,
year = {2020},
author = {Aubier, TG and Galipaud, M and Erten, EY and Kokko, H},
title = {Transmissible cancers and the evolution of sex under the Red Queen hypothesis.},
journal = {PLoS biology},
volume = {18},
number = {11},
pages = {e3000916},
doi = {10.1371/journal.pbio.3000916},
pmid = {33211684},
issn = {1545-7885},
abstract = {The predominance of sexual reproduction in eukaryotes remains paradoxical in evolutionary theory. Of the hypotheses proposed to resolve this paradox, the 'Red Queen hypothesis' emphasises the potential of antagonistic interactions to cause fluctuating selection, which favours the evolution and maintenance of sex. Whereas empirical and theoretical developments have focused on host-parasite interactions, the premises of the Red Queen theory apply equally well to any type of antagonistic interactions. Recently, it has been suggested that early multicellular organisms with basic anticancer defences were presumably plagued by antagonistic interactions with transmissible cancers and that this could have played a pivotal role in the evolution of sex. Here, we dissect this argument using a population genetic model. One fundamental aspect distinguishing transmissible cancers from other parasites is the continual production of cancerous cell lines from hosts' own tissues. We show that this influx dampens fluctuating selection and therefore makes the evolution of sex more difficult than in standard Red Queen models. Although coevolutionary cycling can remain sufficient to select for sex under some parameter regions of our model, we show that the size of those regions shrinks once we account for epidemiological constraints. Altogether, our results suggest that horizontal transmission of cancerous cells is unlikely to cause fluctuating selection favouring sexual reproduction. Nonetheless, we confirm that vertical transmission of cancerous cells can promote the evolution of sex through a separate mechanism, known as similarity selection, that does not depend on coevolutionary fluctuations.},
}
RevDate: 2020-11-17
Central Cell in Flowering Plants: Specification, Signaling, and Evolution.
Frontiers in plant science, 11:590307.
During the reproduction of animals and lower plants, one sperm cell usually outcompetes the rivals to fertilize a single egg cell. But in flowering plants, two sperm cells fertilize the two adjacent dimorphic female gametes, the egg and central cell, respectively, to initiate the embryo and endosperm within a seed. The endosperm nourishes the embryo development and is also the major source of nutrition in cereals for humankind. Central cell as one of the key innovations of flowering plants is the biggest cell in the multicellular haploid female gametophyte (embryo sac). The embryo sac differentiates from the meiotic products through successive events of nuclear divisions, cellularization, and cell specification. Nowadays, accumulating lines of evidence are raveling multiple roles of the central cell rather than only the endosperm precursor. In this review, we summarize the current understanding on its cell fate specification, intercellular communication, and evolution. We also highlight some key unsolved questions for the further studies in this field.
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@article {pmid33193544,
year = {2020},
author = {Li, HJ and Yang, WC},
title = {Central Cell in Flowering Plants: Specification, Signaling, and Evolution.},
journal = {Frontiers in plant science},
volume = {11},
number = {},
pages = {590307},
pmid = {33193544},
issn = {1664-462X},
abstract = {During the reproduction of animals and lower plants, one sperm cell usually outcompetes the rivals to fertilize a single egg cell. But in flowering plants, two sperm cells fertilize the two adjacent dimorphic female gametes, the egg and central cell, respectively, to initiate the embryo and endosperm within a seed. The endosperm nourishes the embryo development and is also the major source of nutrition in cereals for humankind. Central cell as one of the key innovations of flowering plants is the biggest cell in the multicellular haploid female gametophyte (embryo sac). The embryo sac differentiates from the meiotic products through successive events of nuclear divisions, cellularization, and cell specification. Nowadays, accumulating lines of evidence are raveling multiple roles of the central cell rather than only the endosperm precursor. In this review, we summarize the current understanding on its cell fate specification, intercellular communication, and evolution. We also highlight some key unsolved questions for the further studies in this field.},
}
RevDate: 2020-11-17
The Russian Doll Model: How Bacteria Shape Successful and Sustainable Inter-Kingdom Relationships.
Frontiers in microbiology, 11:573759.
Successful inter-kingdom relationships are based upon a dynamic balance between defense and cooperation. A certain degree of competition is necessary to guarantee life spread and development. On the other hand, cooperation is a powerful tool to ensure a long lasting adaptation to changing environmental conditions and to support evolution to a higher level of complexity. Bacteria can interact with their (true or potential) parasites (i.e., phages) and with their multicellular hosts. In these model interactions, bacteria learnt how to cope with their inner and outer host, transforming dangerous signals into opportunities and modulating responses in order to achieve an agreement that is beneficial for the overall participants, thus giving rise to a more complex "organism" or ecosystem. In this review, particular attention will be addressed to underline the minimal energy expenditure required for these successful interactions [e.g., moonlighting proteins, post-translational modifications (PTMs), and multitasking signals] and the systemic vision of these processes and ways of life in which the system proves to be more than the sum of the single components. Using an inside-out perspective, I will examine the possibility of multilevel interactions, in which viruses help bacteria to cope with the animal host and bacteria support the human immune system to counteract viral infection in a circular vision. In this sophisticated network, bacteria represent the precious link that insures system stability with relative low energy expenditure.
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@article {pmid33193180,
year = {2020},
author = {Pessione, E},
title = {The Russian Doll Model: How Bacteria Shape Successful and Sustainable Inter-Kingdom Relationships.},
journal = {Frontiers in microbiology},
volume = {11},
number = {},
pages = {573759},
pmid = {33193180},
issn = {1664-302X},
abstract = {Successful inter-kingdom relationships are based upon a dynamic balance between defense and cooperation. A certain degree of competition is necessary to guarantee life spread and development. On the other hand, cooperation is a powerful tool to ensure a long lasting adaptation to changing environmental conditions and to support evolution to a higher level of complexity. Bacteria can interact with their (true or potential) parasites (i.e., phages) and with their multicellular hosts. In these model interactions, bacteria learnt how to cope with their inner and outer host, transforming dangerous signals into opportunities and modulating responses in order to achieve an agreement that is beneficial for the overall participants, thus giving rise to a more complex "organism" or ecosystem. In this review, particular attention will be addressed to underline the minimal energy expenditure required for these successful interactions [e.g., moonlighting proteins, post-translational modifications (PTMs), and multitasking signals] and the systemic vision of these processes and ways of life in which the system proves to be more than the sum of the single components. Using an inside-out perspective, I will examine the possibility of multilevel interactions, in which viruses help bacteria to cope with the animal host and bacteria support the human immune system to counteract viral infection in a circular vision. In this sophisticated network, bacteria represent the precious link that insures system stability with relative low energy expenditure.},
}
RevDate: 2020-11-13
Do microenvironmental changes disrupt multicellular organisation with ageing, enacting and favouring the cancer cell phenotype?.
BioEssays : news and reviews in molecular, cellular and developmental biology [Epub ahead of print].
Cancer is a singular cellular state, the emergence of which destabilises the homeostasis reached through the evolution to multicellularity. We present the idea that the onset of the cellular disobedience to the metazoan functional and structural architecture, known as the cancer phenotype, is triggered by changes in the cell's external environment that occur with ageing: what ensues is a breach of the social contract of multicellular life characteristic of metazoans. By integrating old ideas with new evidence, we propose that with ageing the environmental information that maintains a multicellular organisation is eroded, rewiring internal processes of the cell, and resulting in an internal shift towards an ancestral condition resulting in the pseudo-multicellular cancer phenotype. Once that phenotype emerges, a new local social contract is built, different from the homeostatic one, leading to tumour formation and the foundation of a novel local ecosystem.
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@article {pmid33184914,
year = {2020},
author = {Castillo, SP and Keymer, JE and Marquet, PA},
title = {Do microenvironmental changes disrupt multicellular organisation with ageing, enacting and favouring the cancer cell phenotype?.},
journal = {BioEssays : news and reviews in molecular, cellular and developmental biology},
volume = {},
number = {},
pages = {e2000126},
doi = {10.1002/bies.202000126},
pmid = {33184914},
issn = {1521-1878},
abstract = {Cancer is a singular cellular state, the emergence of which destabilises the homeostasis reached through the evolution to multicellularity. We present the idea that the onset of the cellular disobedience to the metazoan functional and structural architecture, known as the cancer phenotype, is triggered by changes in the cell's external environment that occur with ageing: what ensues is a breach of the social contract of multicellular life characteristic of metazoans. By integrating old ideas with new evidence, we propose that with ageing the environmental information that maintains a multicellular organisation is eroded, rewiring internal processes of the cell, and resulting in an internal shift towards an ancestral condition resulting in the pseudo-multicellular cancer phenotype. Once that phenotype emerges, a new local social contract is built, different from the homeostatic one, leading to tumour formation and the foundation of a novel local ecosystem.},
}
RevDate: 2020-12-01
Glandular trichomes of Robinia viscosa Vent. var. hartwigii (Koehne) Ashe (Faboideae, Fabaceae)-morphology, histochemistry and ultrastructure.
Planta, 252(6):102.
MAIN CONCLUSION: Permanent glandular trichomes of Robinia viscosa var. hartwigii produce viscous secretion containing several secondary metabolites, as lipids, mucilage, flavonoids, proteins and alkaloids. Robinia viscosa var. hartwigii (Hartweg's locust) is an ornamental tree with high apicultural value. It can be planted in urban greenery and in degraded areas. The shoots, leaves, and inflorescences of this plant are equipped with numerous persistent glandular trichomes producing sticky secretion. The distribution, origin, development, morphology, anatomy, and ultrastructure of glandular trichomes of Hartweg's locust flowers as well as the localisation and composition of their secretory products were investigated for the first time. To this end, light, scanning, and transmission electron microscopy combined with histochemical and fluorescence techniques were used. The massive glandular trichomes differing in the distribution, length, and stage of development were built of a multicellular and multiseriate stalk and a multicellular head. The secretory cells in the stalk and head had large nuclei with nucleoli, numerous chloroplasts with thylakoids and starch grains, mitochondria, endoplasmic reticulum profiles, Golgi apparatus, vesicles, and multivesicular bodies. Many vacuoles contained phenolic compounds dissolved or forming various condensed deposits. The secretion components were transported through symplast elements, and the granulocrine and eccrine modes of nectar secretion were observed. The secretion was accumulated in the subcuticular space at the trichome apex and released through a pore in the cuticle. Histochemical and fluorescence assays showed that the trichomes and secretion contained lipophilic and polyphenol compounds, polysaccharides, proteins, and alkaloids. We suggest that these metabolites may serve an important function in protection of plants against biotic stress conditions and may also be a source of phytopharmaceuticals in the future.
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@article {pmid33180181,
year = {2020},
author = {Konarska, A and Łotocka, B},
title = {Glandular trichomes of Robinia viscosa Vent. var. hartwigii (Koehne) Ashe (Faboideae, Fabaceae)-morphology, histochemistry and ultrastructure.},
journal = {Planta},
volume = {252},
number = {6},
pages = {102},
pmid = {33180181},
issn = {1432-2048},
abstract = {MAIN CONCLUSION: Permanent glandular trichomes of Robinia viscosa var. hartwigii produce viscous secretion containing several secondary metabolites, as lipids, mucilage, flavonoids, proteins and alkaloids. Robinia viscosa var. hartwigii (Hartweg's locust) is an ornamental tree with high apicultural value. It can be planted in urban greenery and in degraded areas. The shoots, leaves, and inflorescences of this plant are equipped with numerous persistent glandular trichomes producing sticky secretion. The distribution, origin, development, morphology, anatomy, and ultrastructure of glandular trichomes of Hartweg's locust flowers as well as the localisation and composition of their secretory products were investigated for the first time. To this end, light, scanning, and transmission electron microscopy combined with histochemical and fluorescence techniques were used. The massive glandular trichomes differing in the distribution, length, and stage of development were built of a multicellular and multiseriate stalk and a multicellular head. The secretory cells in the stalk and head had large nuclei with nucleoli, numerous chloroplasts with thylakoids and starch grains, mitochondria, endoplasmic reticulum profiles, Golgi apparatus, vesicles, and multivesicular bodies. Many vacuoles contained phenolic compounds dissolved or forming various condensed deposits. The secretion components were transported through symplast elements, and the granulocrine and eccrine modes of nectar secretion were observed. The secretion was accumulated in the subcuticular space at the trichome apex and released through a pore in the cuticle. Histochemical and fluorescence assays showed that the trichomes and secretion contained lipophilic and polyphenol compounds, polysaccharides, proteins, and alkaloids. We suggest that these metabolites may serve an important function in protection of plants against biotic stress conditions and may also be a source of phytopharmaceuticals in the future.},
}
RevDate: 2020-11-09
Can natural selection and druggable targets synergize? Of nutrient scarcity, cancer, and the evolution of cooperation.
BioEssays : news and reviews in molecular, cellular and developmental biology [Epub ahead of print].
Since the dawn of molecular biology, cancer therapy has focused on druggable targets. Despite some remarkable successes, cell-level evolution remains a potent antagonist to this approach. We suggest that a deeper understanding of the breakdown of cooperation can synergize the evolutionary and druggable-targets approaches. Complexity requires cooperation, whether between cells of different species (symbiosis) or between cells of the same organism (multicellularity). Both forms of cooperation may be associated with nutrient scarcity, which in turn may be associated with a chemiosmotic metabolism. A variety of examples from modern organisms supports these generalities. Indeed, mammalian cancers-unicellular, glycolytic, and fast-replicating-parallel these examples. Nutrient scarcity, chemiosmosis, and associated signaling may favor cooperation, while under conditions of nutrient abundance a fermentative metabolism may signal the breakdown of cooperation. Manipulating this metabolic milieu may potentiate the effects of targeted therapeutics. Specific opportunities are discussed in this regard, including avicins, a novel plant product.
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@article {pmid33165962,
year = {2020},
author = {Blackstone, NW and Gutterman, JU},
title = {Can natural selection and druggable targets synergize? Of nutrient scarcity, cancer, and the evolution of cooperation.},
journal = {BioEssays : news and reviews in molecular, cellular and developmental biology},
volume = {},
number = {},
pages = {e2000160},
doi = {10.1002/bies.202000160},
pmid = {33165962},
issn = {1521-1878},
abstract = {Since the dawn of molecular biology, cancer therapy has focused on druggable targets. Despite some remarkable successes, cell-level evolution remains a potent antagonist to this approach. We suggest that a deeper understanding of the breakdown of cooperation can synergize the evolutionary and druggable-targets approaches. Complexity requires cooperation, whether between cells of different species (symbiosis) or between cells of the same organism (multicellularity). Both forms of cooperation may be associated with nutrient scarcity, which in turn may be associated with a chemiosmotic metabolism. A variety of examples from modern organisms supports these generalities. Indeed, mammalian cancers-unicellular, glycolytic, and fast-replicating-parallel these examples. Nutrient scarcity, chemiosmosis, and associated signaling may favor cooperation, while under conditions of nutrient abundance a fermentative metabolism may signal the breakdown of cooperation. Manipulating this metabolic milieu may potentiate the effects of targeted therapeutics. Specific opportunities are discussed in this regard, including avicins, a novel plant product.},
}
RevDate: 2020-11-13
Ediacaran Doushantuo-type biota discovered in Laurentia.
Communications biology, 3(1):647.
The Ediacaran period (635-541 Ma) was a time of major environmental change, accompanied by a transition from a microbial world to the animal world we know today. Multicellular, macroscopic organisms preserved as casts and molds in Ediacaran siliciclastic rocks are preserved worldwide and provide snapshots of early organismal, including animal, evolution. Remarkable evolutionary advances are also witnessed by diverse cellular and subcellular phosphatized microfossils described from the Doushantuo Formation in China, the only source showing a diversified assemblage of microfossils. Here, we greatly extend the known distribution of this Doushantuo-type biota in reporting an Ediacaran Lagerstätte from Laurentia (Portfjeld Formation, North Greenland), with phosphatized animal-like eggs, embryos, acritarchs, and cyanobacteria, the age of which is constrained by the Shuram-Wonoka anomaly (c. 570-560 Ma). The discovery of these Ediacaran phosphatized microfossils from outside East Asia extends the distribution of the remarkable biota to a second palaeocontinent in the other hemisphere of the Ediacaran world, considerably expanding our understanding of the temporal and environmental distribution of organisms immediately prior to the Cambrian explosion.
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@article {pmid33159138,
year = {2020},
author = {Willman, S and Peel, JS and Ineson, JR and Schovsbo, NH and Rugen, EJ and Frei, R},
title = {Ediacaran Doushantuo-type biota discovered in Laurentia.},
journal = {Communications biology},
volume = {3},
number = {1},
pages = {647},
pmid = {33159138},
issn = {2399-3642},
abstract = {The Ediacaran period (635-541 Ma) was a time of major environmental change, accompanied by a transition from a microbial world to the animal world we know today. Multicellular, macroscopic organisms preserved as casts and molds in Ediacaran siliciclastic rocks are preserved worldwide and provide snapshots of early organismal, including animal, evolution. Remarkable evolutionary advances are also witnessed by diverse cellular and subcellular phosphatized microfossils described from the Doushantuo Formation in China, the only source showing a diversified assemblage of microfossils. Here, we greatly extend the known distribution of this Doushantuo-type biota in reporting an Ediacaran Lagerstätte from Laurentia (Portfjeld Formation, North Greenland), with phosphatized animal-like eggs, embryos, acritarchs, and cyanobacteria, the age of which is constrained by the Shuram-Wonoka anomaly (c. 570-560 Ma). The discovery of these Ediacaran phosphatized microfossils from outside East Asia extends the distribution of the remarkable biota to a second palaeocontinent in the other hemisphere of the Ediacaran world, considerably expanding our understanding of the temporal and environmental distribution of organisms immediately prior to the Cambrian explosion.},
}
RevDate: 2020-11-20
CmpDate: 2020-11-20
[Environment and immunity-Allergies and autoimmune diseases from epidemiological perspective].
Nihon eiseigaku zasshi. Japanese journal of hygiene, 75(0):.
Immunity, which denotes the protection of multicellular organisms against various bacterial and viral infections, is an essential protective mechanism for living organisms. Allergy is a reaction to a foreign substance existing in the environment that is basically not a component of the self. Additionally, autoimmune diseases are associated with the dysfunction in the recognition of self and non-self, and are pathological conditions caused by immune cells attacking their own tissues and cells. In this paper, we outline the current status of immunity with respect to the environment from the epidemiological perspective with regard to the following: (1) evolution and immunity, (2) allergy, (3) autoantibodies, (4) autoimmune diseases, (5) relationships of immunity with the environment, allergy, autoantibodies, and autoimmune diseases, and (6) celiac disease.
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@article {pmid33148926,
year = {2020},
author = {Katoh, T and Satoh, M},
title = {[Environment and immunity-Allergies and autoimmune diseases from epidemiological perspective].},
journal = {Nihon eiseigaku zasshi. Japanese journal of hygiene},
volume = {75},
number = {0},
pages = {},
doi = {10.1265/jjh.20005},
pmid = {33148926},
issn = {1882-6482},
mesh = {Adolescent ; Adult ; Aged ; Autoantibodies ; Autoimmune Diseases/epidemiology/*immunology ; *Autoimmunity ; Biological Evolution ; Celiac Disease/immunology ; Child ; Child, Preschool ; Environment ; Female ; Humans ; Hypersensitivity/epidemiology/*immunology ; Infant ; Male ; Middle Aged ; Young Adult ; },
abstract = {Immunity, which denotes the protection of multicellular organisms against various bacterial and viral infections, is an essential protective mechanism for living organisms. Allergy is a reaction to a foreign substance existing in the environment that is basically not a component of the self. Additionally, autoimmune diseases are associated with the dysfunction in the recognition of self and non-self, and are pathological conditions caused by immune cells attacking their own tissues and cells. In this paper, we outline the current status of immunity with respect to the environment from the epidemiological perspective with regard to the following: (1) evolution and immunity, (2) allergy, (3) autoantibodies, (4) autoimmune diseases, (5) relationships of immunity with the environment, allergy, autoantibodies, and autoimmune diseases, and (6) celiac disease.},
}
MeSH Terms:
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Adolescent
Adult
Aged
Autoantibodies
Autoimmune Diseases/epidemiology/*immunology
*Autoimmunity
Biological Evolution
Celiac Disease/immunology
Child
Child, Preschool
Environment
Female
Humans
Hypersensitivity/epidemiology/*immunology
Infant
Male
Middle Aged
Young Adult
RevDate: 2020-11-28
CancerGram: An Effective Classifier for Differentiating Anticancer from Antimicrobial Peptides.
Pharmaceutics, 12(11):.
Antimicrobial peptides (AMPs) constitute a diverse group of bioactive molecules that provide multicellular organisms with protection against microorganisms, and microorganisms with weaponry for competition. Some AMPs can target cancer cells; thus, they are called anticancer peptides (ACPs). Due to their small size, positive charge, hydrophobicity and amphipathicity, AMPs and ACPs interact with negatively charged components of biological membranes. AMPs preferentially permeabilize microbial membranes, but ACPs additionally target mitochondrial and plasma membranes of cancer cells. The preference towards mitochondrial membranes is explained by their membrane potential, membrane composition resulting from α-proteobacterial origin and the fact that mitochondrial targeting signals could have evolved from AMPs. Taking into account the therapeutic potential of ACPs and millions of deaths due to cancer annually, it is of vital importance to find new cationic peptides that selectively destroy cancer cells. Therefore, to reduce the costs of experimental research, we have created a robust computational tool, CancerGram, that uses n-grams and random forests for predicting ACPs. Compared to other ACP classifiers, CancerGram is the first three-class model that effectively classifies peptides into: ACPs, AMPs and non-ACPs/non-AMPs, with AU1U amounting to 0.89 and a Kappa statistic of 0.65. CancerGram is available as a web server and R package on GitHub.
Additional Links: PMID-33142753
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@article {pmid33142753,
year = {2020},
author = {Burdukiewicz, M and Sidorczuk, K and Rafacz, D and Pietluch, F and Bąkała, M and Słowik, J and Gagat, P},
title = {CancerGram: An Effective Classifier for Differentiating Anticancer from Antimicrobial Peptides.},
journal = {Pharmaceutics},
volume = {12},
number = {11},
pages = {},
pmid = {33142753},
issn = {1999-4923},
support = {2017/26/D/NZ8/00444//Narodowym Centrum Nauki/ ; 2018/31/N/NZ2/01338//Narodowym Centrum Nauki/ ; 2019/35/N/NZ8/03366//Narodowym Centrum Nauki/ ; },
abstract = {Antimicrobial peptides (AMPs) constitute a diverse group of bioactive molecules that provide multicellular organisms with protection against microorganisms, and microorganisms with weaponry for competition. Some AMPs can target cancer cells; thus, they are called anticancer peptides (ACPs). Due to their small size, positive charge, hydrophobicity and amphipathicity, AMPs and ACPs interact with negatively charged components of biological membranes. AMPs preferentially permeabilize microbial membranes, but ACPs additionally target mitochondrial and plasma membranes of cancer cells. The preference towards mitochondrial membranes is explained by their membrane potential, membrane composition resulting from α-proteobacterial origin and the fact that mitochondrial targeting signals could have evolved from AMPs. Taking into account the therapeutic potential of ACPs and millions of deaths due to cancer annually, it is of vital importance to find new cationic peptides that selectively destroy cancer cells. Therefore, to reduce the costs of experimental research, we have created a robust computational tool, CancerGram, that uses n-grams and random forests for predicting ACPs. Compared to other ACP classifiers, CancerGram is the first three-class model that effectively classifies peptides into: ACPs, AMPs and non-ACPs/non-AMPs, with AU1U amounting to 0.89 and a Kappa statistic of 0.65. CancerGram is available as a web server and R package on GitHub.},
}
RevDate: 2020-11-03
Evolution of Multicellularity: One from Many or Many from One?.
Current biology : CB, 30(21):R1306-R1308.
Multicellularity has evolved many times. A new study explores why some forms of multicellularity may be better than others.
Additional Links: PMID-33142097
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@article {pmid33142097,
year = {2020},
author = {Ostrowski, EA},
title = {Evolution of Multicellularity: One from Many or Many from One?.},
journal = {Current biology : CB},
volume = {30},
number = {21},
pages = {R1306-R1308},
doi = {10.1016/j.cub.2020.08.056},
pmid = {33142097},
issn = {1879-0445},
abstract = {Multicellularity has evolved many times. A new study explores why some forms of multicellularity may be better than others.},
}
RevDate: 2020-11-16
CmpDate: 2020-11-16
How geometry shapes division of labor.
eLife, 9:.
A mathematical model shows how the shape of early multicellular organisms may have helped cells evolve specialized roles.
Additional Links: PMID-33140720
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@article {pmid33140720,
year = {2020},
author = {Staps, M and Tarnita, C},
title = {How geometry shapes division of labor.},
journal = {eLife},
volume = {9},
number = {},
pages = {},
pmid = {33140720},
issn = {2050-084X},
mesh = {*Biological Evolution ; *Models, Biological ; Reproduction ; },
abstract = {A mathematical model shows how the shape of early multicellular organisms may have helped cells evolve specialized roles.},
}
MeSH Terms:
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*Biological Evolution
*Models, Biological
Reproduction
RevDate: 2020-11-28
The Plant Target of Rapamycin: A Conduc TOR of Nutrition and Metabolism in Photosynthetic Organisms.
Genes, 11(11):.
Living organisms possess many mechanisms to sense nutrients and favorable conditions, which allow them to grow and develop. Photosynthetic organisms are very diverse, from green unicellular algae to multicellular flowering plants, but most of them are sessile and thus unable to escape from the biotic and abiotic stresses they experience. The Target of Rapamycin (TOR) signaling pathway is conserved in all eukaryotes and acts as a central regulatory hub between growth and extrinsic factors, such as nutrients or stress. However, relatively little is known about the regulations and roles of this pathway in plants and algae. Although some features of the TOR pathway seem to have been highly conserved throughout evolution, others clearly differ in plants, perhaps reflecting adaptations to different lifestyles and the rewiring of this primordial signaling module to adapt to specific requirements. Indeed, TOR is involved in plant responses to a vast array of signals including nutrients, hormones, light, stresses or pathogens. In this review, we will summarize recent studies that address the regulations of TOR by nutrients in photosynthetic organisms, and the roles of TOR in controlling important metabolic pathways, highlighting similarities and differences with the other eukaryotes.
Additional Links: PMID-33138108
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@article {pmid33138108,
year = {2020},
author = {Ingargiola, C and Turqueto Duarte, G and Robaglia, C and Leprince, AS and Meyer, C},
title = {The Plant Target of Rapamycin: A Conduc TOR of Nutrition and Metabolism in Photosynthetic Organisms.},
journal = {Genes},
volume = {11},
number = {11},
pages = {},
pmid = {33138108},
issn = {2073-4425},
support = {ECO201806006346//Fondation pour la Recherche Médicale/ ; ANR-17-EUR-0007, EUR SPS-GSR//Agence Nationale de la Recherche/ ; FP7-609398//Seventh Framework Programme/ ; },
abstract = {Living organisms possess many mechanisms to sense nutrients and favorable conditions, which allow them to grow and develop. Photosynthetic organisms are very diverse, from green unicellular algae to multicellular flowering plants, but most of them are sessile and thus unable to escape from the biotic and abiotic stresses they experience. The Target of Rapamycin (TOR) signaling pathway is conserved in all eukaryotes and acts as a central regulatory hub between growth and extrinsic factors, such as nutrients or stress. However, relatively little is known about the regulations and roles of this pathway in plants and algae. Although some features of the TOR pathway seem to have been highly conserved throughout evolution, others clearly differ in plants, perhaps reflecting adaptations to different lifestyles and the rewiring of this primordial signaling module to adapt to specific requirements. Indeed, TOR is involved in plant responses to a vast array of signals including nutrients, hormones, light, stresses or pathogens. In this review, we will summarize recent studies that address the regulations of TOR by nutrients in photosynthetic organisms, and the roles of TOR in controlling important metabolic pathways, highlighting similarities and differences with the other eukaryotes.},
}
RevDate: 2020-11-03
Expanding magnetic organelle biogenesis in the domain Bacteria.
Microbiome, 8(1):152.
BACKGROUND: The discovery of membrane-enclosed, metabolically functional organelles in Bacteria has transformed our understanding of the subcellular complexity of prokaryotic cells. Biomineralization of magnetic nanoparticles within magnetosomes by magnetotactic bacteria (MTB) is a fascinating example of prokaryotic organelles. Magnetosomes, as nano-sized magnetic sensors in MTB, facilitate cell navigation along the local geomagnetic field, a behaviour referred to as magnetotaxis or microbial magnetoreception. Recent discovery of novel MTB outside the traditionally recognized taxonomic lineages suggests that MTB diversity across the domain Bacteria are considerably underestimated, which limits understanding of the taxonomic distribution and evolutionary origin of magnetosome organelle biogenesis.
RESULTS: Here, we perform the most comprehensive metagenomic analysis available of MTB communities and reconstruct metagenome-assembled MTB genomes from diverse ecosystems. Discovery of MTB in acidic peatland soils suggests widespread MTB occurrence in waterlogged soils in addition to subaqueous sediments and water bodies. A total of 168 MTB draft genomes have been reconstructed, which represent nearly a 3-fold increase over the number currently available and more than double the known MTB species at the genome level. Phylogenomic analysis reveals that these genomes belong to 13 Bacterial phyla, six of which were previously not known to include MTB. These findings indicate a much wider taxonomic distribution of magnetosome organelle biogenesis across the domain Bacteria than previously thought. Comparative genome analysis reveals a vast diversity of magnetosome gene clusters involved in magnetosomal biogenesis in terms of gene content and synteny residing in distinct taxonomic lineages. Phylogenetic analyses of core magnetosome proteins in this largest available and taxonomically diverse dataset support an unexpectedly early evolutionary origin of magnetosome biomineralization, likely ancestral to the origin of the domain Bacteria.
CONCLUSIONS: These findings expand the taxonomic and phylogenetic diversity of MTB across the domain Bacteria and shed new light on the origin and evolution of microbial magnetoreception. Potential biogenesis of the magnetosome organelle in the close descendants of the last bacterial common ancestor has important implications for our understanding of the evolutionary history of bacterial cellular complexity and emphasizes the biological significance of the magnetosome organelle. Video Abstract.
Additional Links: PMID-33126926
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@article {pmid33126926,
year = {2020},
author = {Lin, W and Zhang, W and Paterson, GA and Zhu, Q and Zhao, X and Knight, R and Bazylinski, DA and Roberts, AP and Pan, Y},
title = {Expanding magnetic organelle biogenesis in the domain Bacteria.},
journal = {Microbiome},
volume = {8},
number = {1},
pages = {152},
pmid = {33126926},
issn = {2049-2618},
abstract = {BACKGROUND: The discovery of membrane-enclosed, metabolically functional organelles in Bacteria has transformed our understanding of the subcellular complexity of prokaryotic cells. Biomineralization of magnetic nanoparticles within magnetosomes by magnetotactic bacteria (MTB) is a fascinating example of prokaryotic organelles. Magnetosomes, as nano-sized magnetic sensors in MTB, facilitate cell navigation along the local geomagnetic field, a behaviour referred to as magnetotaxis or microbial magnetoreception. Recent discovery of novel MTB outside the traditionally recognized taxonomic lineages suggests that MTB diversity across the domain Bacteria are considerably underestimated, which limits understanding of the taxonomic distribution and evolutionary origin of magnetosome organelle biogenesis.
RESULTS: Here, we perform the most comprehensive metagenomic analysis available of MTB communities and reconstruct metagenome-assembled MTB genomes from diverse ecosystems. Discovery of MTB in acidic peatland soils suggests widespread MTB occurrence in waterlogged soils in addition to subaqueous sediments and water bodies. A total of 168 MTB draft genomes have been reconstructed, which represent nearly a 3-fold increase over the number currently available and more than double the known MTB species at the genome level. Phylogenomic analysis reveals that these genomes belong to 13 Bacterial phyla, six of which were previously not known to include MTB. These findings indicate a much wider taxonomic distribution of magnetosome organelle biogenesis across the domain Bacteria than previously thought. Comparative genome analysis reveals a vast diversity of magnetosome gene clusters involved in magnetosomal biogenesis in terms of gene content and synteny residing in distinct taxonomic lineages. Phylogenetic analyses of core magnetosome proteins in this largest available and taxonomically diverse dataset support an unexpectedly early evolutionary origin of magnetosome biomineralization, likely ancestral to the origin of the domain Bacteria.
CONCLUSIONS: These findings expand the taxonomic and phylogenetic diversity of MTB across the domain Bacteria and shed new light on the origin and evolution of microbial magnetoreception. Potential biogenesis of the magnetosome organelle in the close descendants of the last bacterial common ancestor has important implications for our understanding of the evolutionary history of bacterial cellular complexity and emphasizes the biological significance of the magnetosome organelle. Video Abstract.},
}
RevDate: 2020-11-14
Cell Communications among Microorganisms, Plants, and Animals: Origin, Evolution, and Interplays.
International journal of molecular sciences, 21(21):.
Cellular communications play pivotal roles in multi-cellular species, but they do so also in uni-cellular species. Moreover, cells communicate with each other not only within the same individual, but also with cells in other individuals belonging to the same or other species. These communications occur between two unicellular species, two multicellular species, or between unicellular and multicellular species. The molecular mechanisms involved exhibit diversity and specificity, but they share common basic features, which allow common pathways of communication between different species, often phylogenetically very distant. These interactions are possible by the high degree of conservation of the basic molecular mechanisms of interaction of many ligand-receptor pairs in evolutionary remote species. These inter-species cellular communications played crucial roles during Evolution and must have been positively selected, particularly when collectively beneficial in hostile environments. It is likely that communications between cells did not arise after their emergence, but were part of the very nature of the first cells. Synchronization of populations of non-living protocells through chemical communications may have been a mandatory step towards their emergence as populations of living cells and explain the large commonality of cell communication mechanisms among microorganisms, plants, and animals.
Additional Links: PMID-33126770
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@article {pmid33126770,
year = {2020},
author = {Combarnous, Y and Nguyen, TMD},
title = {Cell Communications among Microorganisms, Plants, and Animals: Origin, Evolution, and Interplays.},
journal = {International journal of molecular sciences},
volume = {21},
number = {21},
pages = {},
pmid = {33126770},
issn = {1422-0067},
abstract = {Cellular communications play pivotal roles in multi-cellular species, but they do so also in uni-cellular species. Moreover, cells communicate with each other not only within the same individual, but also with cells in other individuals belonging to the same or other species. These communications occur between two unicellular species, two multicellular species, or between unicellular and multicellular species. The molecular mechanisms involved exhibit diversity and specificity, but they share common basic features, which allow common pathways of communication between different species, often phylogenetically very distant. These interactions are possible by the high degree of conservation of the basic molecular mechanisms of interaction of many ligand-receptor pairs in evolutionary remote species. These inter-species cellular communications played crucial roles during Evolution and must have been positively selected, particularly when collectively beneficial in hostile environments. It is likely that communications between cells did not arise after their emergence, but were part of the very nature of the first cells. Synchronization of populations of non-living protocells through chemical communications may have been a mandatory step towards their emergence as populations of living cells and explain the large commonality of cell communication mechanisms among microorganisms, plants, and animals.},
}
RevDate: 2020-11-28
Intrinsically Disordered Proteins: Insights from Poincaré, Waddington, and Lamarck.
Biomolecules, 10(11):.
The past quarter-century may justly be referred to as a period analogous to the "Cambrian explosion" in the history of proteins. This period is marked by the appearance of the intrinsically disordered proteins (IDPs) on the scene since their discovery in the mid-1990s. Here, I first reflect on how we accidentally stumbled on these fascinating molecules. Next, I describe our research on the IDPs over the past decade and identify six areas as important for future research in this field. In addition, I draw on discoveries others in the field have made to present a more comprehensive essay. More specifically, I discuss the role of IDPs in two fundamental aspects of life: in phenotypic switching, and in multicellularity that marks one of the major evolutionary transitions. I highlight how serendipity, imagination, and an interdisciplinary approach embodying empirical evidence and theoretical insights from the works of Poincaré, Waddington, and Lamarck, shaped our thinking, and how this led us to propose the MRK hypothesis, a conceptual framework addressing phenotypic switching, the emergence of new traits, and adaptive evolution via nongenetic and IDP conformation-based mechanisms. Finally, I present a perspective on the evolutionary link between phenotypic switching and the origin of multicellularity.
Additional Links: PMID-33126482
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@article {pmid33126482,
year = {2020},
author = {Kulkarni, P},
title = {Intrinsically Disordered Proteins: Insights from Poincaré, Waddington, and Lamarck.},
journal = {Biomolecules},
volume = {10},
number = {11},
pages = {},
pmid = {33126482},
issn = {2218-273X},
abstract = {The past quarter-century may justly be referred to as a period analogous to the "Cambrian explosion" in the history of proteins. This period is marked by the appearance of the intrinsically disordered proteins (IDPs) on the scene since their discovery in the mid-1990s. Here, I first reflect on how we accidentally stumbled on these fascinating molecules. Next, I describe our research on the IDPs over the past decade and identify six areas as important for future research in this field. In addition, I draw on discoveries others in the field have made to present a more comprehensive essay. More specifically, I discuss the role of IDPs in two fundamental aspects of life: in phenotypic switching, and in multicellularity that marks one of the major evolutionary transitions. I highlight how serendipity, imagination, and an interdisciplinary approach embodying empirical evidence and theoretical insights from the works of Poincaré, Waddington, and Lamarck, shaped our thinking, and how this led us to propose the MRK hypothesis, a conceptual framework addressing phenotypic switching, the emergence of new traits, and adaptive evolution via nongenetic and IDP conformation-based mechanisms. Finally, I present a perspective on the evolutionary link between phenotypic switching and the origin of multicellularity.},
}
RevDate: 2020-10-30
Vesicle Transport in Plants: A Revised Phylogeny of SNARE Proteins.
Evolutionary bioinformatics online, 16:1176934320956575.
Communication systems within and between plant cells involve the transfer of ions and molecules between compartments, and are essential for development and responses to biotic and abiotic stresses. This in turn requires the regulated movement and fusion of membrane systems with their associated cargo. Recent advances in genomics has provided new resources with which to investigate the evolutionary relationships between membrane proteins across plant species. Members of the soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) are known to play important roles in vesicle trafficking across plant, animal and microbial species. Using recent public expression and transcriptomic data from 9 representative green plants, we investigated the evolution of the SNARE classes and linked protein changes to functional specialization (expression patterns). We identified an additional 3 putative SNARE genes in the model plant Arabidopsis. We found that all SNARE classes have expanded in number to a greater or lesser degree alongside the evolution of multicellularity, and that within-species expansions are also common. These gene expansions appear to be associated with the accumulation of amino acid changes and with sub-functionalization of SNARE family members to different tissues. These results provide an insight into SNARE protein evolution and functional specialization. The work provides a platform for hypothesis-building and future research into the precise functions of these proteins in plant development and responses to the environment.
Additional Links: PMID-33116351
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@article {pmid33116351,
year = {2020},
author = {Gu, X and Brennan, A and Wei, W and Guo, G and Lindsey, K},
title = {Vesicle Transport in Plants: A Revised Phylogeny of SNARE Proteins.},
journal = {Evolutionary bioinformatics online},
volume = {16},
number = {},
pages = {1176934320956575},
pmid = {33116351},
issn = {1176-9343},
abstract = {Communication systems within and between plant cells involve the transfer of ions and molecules between compartments, and are essential for development and responses to biotic and abiotic stresses. This in turn requires the regulated movement and fusion of membrane systems with their associated cargo. Recent advances in genomics has provided new resources with which to investigate the evolutionary relationships between membrane proteins across plant species. Members of the soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) are known to play important roles in vesicle trafficking across plant, animal and microbial species. Using recent public expression and transcriptomic data from 9 representative green plants, we investigated the evolution of the SNARE classes and linked protein changes to functional specialization (expression patterns). We identified an additional 3 putative SNARE genes in the model plant Arabidopsis. We found that all SNARE classes have expanded in number to a greater or lesser degree alongside the evolution of multicellularity, and that within-species expansions are also common. These gene expansions appear to be associated with the accumulation of amino acid changes and with sub-functionalization of SNARE family members to different tissues. These results provide an insight into SNARE protein evolution and functional specialization. The work provides a platform for hypothesis-building and future research into the precise functions of these proteins in plant development and responses to the environment.},
}
RevDate: 2020-11-27
Phyllotaxis from a Single Apical Cell.
Trends in plant science pii:S1360-1385(20)30292-2 [Epub ahead of print].
Phyllotaxis, the geometry of leaf arrangement around stems, determines plant architecture. Molecular interactions coordinating the formation of phyllotactic patterns have mainly been studied in multicellular shoot apical meristems of flowering plants. Phyllotaxis evolved independently in the major land plant lineages. In mosses, it arises from a single apical cell, raising the question of how asymmetric divisions of a single-celled meristem create phyllotactic patterns and whether associated genetic processes are shared across lineages. We present an overview of the mechanisms governing shoot apical cell specification and activity in the model moss, Physcomitrium patens, and argue that similar molecular regulatory modules have been deployed repeatedly across evolution to operate at different scales and drive apical function in convergent shoot forms.
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@article {pmid33097400,
year = {2020},
author = {Véron, E and Vernoux, T and Coudert, Y},
title = {Phyllotaxis from a Single Apical Cell.},
journal = {Trends in plant science},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tplants.2020.09.014},
pmid = {33097400},
issn = {1878-4372},
abstract = {Phyllotaxis, the geometry of leaf arrangement around stems, determines plant architecture. Molecular interactions coordinating the formation of phyllotactic patterns have mainly been studied in multicellular shoot apical meristems of flowering plants. Phyllotaxis evolved independently in the major land plant lineages. In mosses, it arises from a single apical cell, raising the question of how asymmetric divisions of a single-celled meristem create phyllotactic patterns and whether associated genetic processes are shared across lineages. We present an overview of the mechanisms governing shoot apical cell specification and activity in the model moss, Physcomitrium patens, and argue that similar molecular regulatory modules have been deployed repeatedly across evolution to operate at different scales and drive apical function in convergent shoot forms.},
}
RevDate: 2020-11-20
Regeneration in the sponge Sycon ciliatum partly mimics postlarval development.
Development (Cambridge, England), 147(22): pii:dev.193714.
Somatic cells dissociated from an adult sponge can reorganize and develop into a juvenile-like sponge, a remarkable phenomenon of regeneration. However, the extent to which regeneration recapitulates embryonic developmental pathways has remained enigmatic. We have standardized and established a sponge Sycon ciliatum regeneration protocol from dissociated cells. Morphological analysis demonstrated that dissociated sponge cells follow a series of morphological events resembling postembryonic development. We performed high-throughput sequencing on regenerating samples and compared the data with that from regular postlarval development. Our comparative transcriptomic analysis revealed that sponge regeneration is as equally dynamic as embryogenesis. We found that sponge regeneration is orchestrated by recruiting pathways similar to those utilized in embryonic development. We also demonstrated that sponge regeneration is accompanied by cell death at early stages, revealing the importance of apoptosis in remodelling the primmorphs to initiate re-development. Because sponges are likely to be the first branch of extant multicellular animals, we suggest that this system can be explored to study the genetic features underlying the evolution of multicellularity and regeneration.
Additional Links: PMID-33093150
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@article {pmid33093150,
year = {2020},
author = {Soubigou, A and Ross, EG and Touhami, Y and Chrismas, N and Modepalli, V},
title = {Regeneration in the sponge Sycon ciliatum partly mimics postlarval development.},
journal = {Development (Cambridge, England)},
volume = {147},
number = {22},
pages = {},
doi = {10.1242/dev.193714},
pmid = {33093150},
issn = {1477-9129},
abstract = {Somatic cells dissociated from an adult sponge can reorganize and develop into a juvenile-like sponge, a remarkable phenomenon of regeneration. However, the extent to which regeneration recapitulates embryonic developmental pathways has remained enigmatic. We have standardized and established a sponge Sycon ciliatum regeneration protocol from dissociated cells. Morphological analysis demonstrated that dissociated sponge cells follow a series of morphological events resembling postembryonic development. We performed high-throughput sequencing on regenerating samples and compared the data with that from regular postlarval development. Our comparative transcriptomic analysis revealed that sponge regeneration is as equally dynamic as embryogenesis. We found that sponge regeneration is orchestrated by recruiting pathways similar to those utilized in embryonic development. We also demonstrated that sponge regeneration is accompanied by cell death at early stages, revealing the importance of apoptosis in remodelling the primmorphs to initiate re-development. Because sponges are likely to be the first branch of extant multicellular animals, we suggest that this system can be explored to study the genetic features underlying the evolution of multicellularity and regeneration.},
}
RevDate: 2020-10-27
Oxygen-sensing mechanisms across eukaryotic kingdoms and their roles in complex multicellularity.
Science (New York, N.Y.), 370(6515):.
Oxygen-sensing mechanisms of eukaryotic multicellular organisms coordinate hypoxic cellular responses in a spatiotemporal manner. Although this capacity partly allows animals and plants to acutely adapt to oxygen deprivation, its functional and historical roots in hypoxia emphasize a broader evolutionary role. For multicellular life-forms that persist in settings with variable oxygen concentrations, the capacity to perceive and modulate responses in and between cells is pivotal. Animals and higher plants represent the most complex life-forms that ever diversified on Earth, and their oxygen-sensing mechanisms demonstrate convergent evolution from a functional perspective. Exploring oxygen-sensing mechanisms across eukaryotic kingdoms can inform us on biological innovations to harness ever-changing oxygen availability at the dawn of complex life and its utilization for their organismal development.
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@article {pmid33093080,
year = {2020},
author = {Hammarlund, EU and Flashman, E and Mohlin, S and Licausi, F},
title = {Oxygen-sensing mechanisms across eukaryotic kingdoms and their roles in complex multicellularity.},
journal = {Science (New York, N.Y.)},
volume = {370},
number = {6515},
pages = {},
doi = {10.1126/science.aba3512},
pmid = {33093080},
issn = {1095-9203},
abstract = {Oxygen-sensing mechanisms of eukaryotic multicellular organisms coordinate hypoxic cellular responses in a spatiotemporal manner. Although this capacity partly allows animals and plants to acutely adapt to oxygen deprivation, its functional and historical roots in hypoxia emphasize a broader evolutionary role. For multicellular life-forms that persist in settings with variable oxygen concentrations, the capacity to perceive and modulate responses in and between cells is pivotal. Animals and higher plants represent the most complex life-forms that ever diversified on Earth, and their oxygen-sensing mechanisms demonstrate convergent evolution from a functional perspective. Exploring oxygen-sensing mechanisms across eukaryotic kingdoms can inform us on biological innovations to harness ever-changing oxygen availability at the dawn of complex life and its utilization for their organismal development.},
}
RevDate: 2020-10-20
The Distribution of Genes Associated With Regulated Cell Death Is Decoupled From the Mitochondrial Phenotypes Within Unicellular Eukaryotic Hosts.
Frontiers in cell and developmental biology, 8:536389.
Genetically regulated cell death (RCD) occurs in all domains of life. In eukaryotes, the evolutionary origin of the mitochondrion and of certain forms of RCD, in particular apoptosis, are thought to coincide, suggesting a central general role for mitochondria in cellular suicide. We tested this mitochondrial centrality hypothesis across a dataset of 67 species of protists, presenting 5 classes of mitochondrial phenotypes, including functional mitochondria, metabolically diversified mitochondria, functionally reduced mitochondria (Mitochondrion Related Organelle or MRO) and even complete absence of mitochondria. We investigated the distribution of genes associated with various forms of RCD. No homologs for described mammalian regulators of regulated necrosis could be identified in our set of 67 unicellular taxa. Protists with MRO and the secondarily a mitochondriate Monocercomonoides exilis display heterogeneous reductions of apoptosis gene sets with respect to typical mitochondriate protists. Remarkably, despite the total lack of mitochondria in M. exilis, apoptosis-associated genes could still be identified. These same species of protists with MRO and M. exilis harbored non-reduced autophagic cell death gene sets. Moreover, transiently multicellular protist taxa appeared enriched in apoptotic and autophagy associated genes compared to free-living protists. This analysis suggests that genes associated with apoptosis in animals and the presence of the mitochondria are significant yet non-essential biological components for RCD in protists. More generally, our results support the hypothesis of a selection for RCD, including both apoptosis and autophagy, as a developmental mechanism linked to multicellularity.
Additional Links: PMID-33072737
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@article {pmid33072737,
year = {2020},
author = {Teulière, J and Bernard, G and Bapteste, E},
title = {The Distribution of Genes Associated With Regulated Cell Death Is Decoupled From the Mitochondrial Phenotypes Within Unicellular Eukaryotic Hosts.},
journal = {Frontiers in cell and developmental biology},
volume = {8},
number = {},
pages = {536389},
pmid = {33072737},
issn = {2296-634X},
abstract = {Genetically regulated cell death (RCD) occurs in all domains of life. In eukaryotes, the evolutionary origin of the mitochondrion and of certain forms of RCD, in particular apoptosis, are thought to coincide, suggesting a central general role for mitochondria in cellular suicide. We tested this mitochondrial centrality hypothesis across a dataset of 67 species of protists, presenting 5 classes of mitochondrial phenotypes, including functional mitochondria, metabolically diversified mitochondria, functionally reduced mitochondria (Mitochondrion Related Organelle or MRO) and even complete absence of mitochondria. We investigated the distribution of genes associated with various forms of RCD. No homologs for described mammalian regulators of regulated necrosis could be identified in our set of 67 unicellular taxa. Protists with MRO and the secondarily a mitochondriate Monocercomonoides exilis display heterogeneous reductions of apoptosis gene sets with respect to typical mitochondriate protists. Remarkably, despite the total lack of mitochondria in M. exilis, apoptosis-associated genes could still be identified. These same species of protists with MRO and M. exilis harbored non-reduced autophagic cell death gene sets. Moreover, transiently multicellular protist taxa appeared enriched in apoptotic and autophagy associated genes compared to free-living protists. This analysis suggests that genes associated with apoptosis in animals and the presence of the mitochondria are significant yet non-essential biological components for RCD in protists. More generally, our results support the hypothesis of a selection for RCD, including both apoptosis and autophagy, as a developmental mechanism linked to multicellularity.},
}
RevDate: 2020-11-27
Functional Long Non-coding RNAs Evolve from Junk Transcripts.
Cell, 183(5):1151-1161.
Transcriptome studies reveal pervasive transcription of complex genomes, such as those of mammals. Despite popular arguments for functionality of most, if not all, of these transcripts, genome-wide analysis of selective constraints indicates that most of the produced RNA are junk. However, junk is not garbage. On the contrary, junk transcripts provide the raw material for the evolution of diverse long non-coding (lnc) RNAs by non-adaptive mechanisms, such as constructive neutral evolution. The generation of many novel functional entities, such as lncRNAs, that fuels organismal complexity does not seem to be driven by strong positive selection. Rather, the weak selection regime that dominates the evolution of most multicellular eukaryotes provides ample material for functional innovation with relatively little adaptation involved.
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@article {pmid33068526,
year = {2020},
author = {Palazzo, AF and Koonin, EV},
title = {Functional Long Non-coding RNAs Evolve from Junk Transcripts.},
journal = {Cell},
volume = {183},
number = {5},
pages = {1151-1161},
doi = {10.1016/j.cell.2020.09.047},
pmid = {33068526},
issn = {1097-4172},
abstract = {Transcriptome studies reveal pervasive transcription of complex genomes, such as those of mammals. Despite popular arguments for functionality of most, if not all, of these transcripts, genome-wide analysis of selective constraints indicates that most of the produced RNA are junk. However, junk is not garbage. On the contrary, junk transcripts provide the raw material for the evolution of diverse long non-coding (lnc) RNAs by non-adaptive mechanisms, such as constructive neutral evolution. The generation of many novel functional entities, such as lncRNAs, that fuels organismal complexity does not seem to be driven by strong positive selection. Rather, the weak selection regime that dominates the evolution of most multicellular eukaryotes provides ample material for functional innovation with relatively little adaptation involved.},
}
RevDate: 2020-11-26
CmpDate: 2020-11-26
Transcriptome data reveal conserved patterns of fruiting body development and response to heat stress in the mushroom-forming fungus Flammulina filiformis.
PloS one, 15(10):e0239890.
Mushroom-forming fungi are complex multicellular organisms that form the basis of a large industry, yet, our understanding of the mechanisms of mushroom development and its responses to various stresses remains limited. The winter mushroom (Flammulina filiformis) is cultivated at a large commercial scale in East Asia and is a species with a preference for low temperatures. This study investigated fruiting body development in F. filiformis by comparing transcriptomes of 4 developmental stages, and compared the developmental genes to a 200-genome dataset to identify conserved genes involved in fruiting body development, and examined the response of heat sensitive and -resistant strains to heat stress. Our data revealed widely conserved genes involved in primordium development of F. filiformis, many of which originated before the emergence of the Agaricomycetes, indicating co-option for complex multicellularity during evolution. We also revealed several notable fruiting-specific genes, including the genes with conserved stipe-specific expression patterns and the others which related to sexual development, water absorption, basidium formation and sporulation, among others. Comparative analysis revealed that heat stress induced more genes in the heat resistant strain (M1) than in the heat sensitive one (XR). Of particular importance are the hsp70, hsp90 and fes1 genes, which may facilitate the adjustment to heat stress in the early stages of fruiting body development. These data highlighted novel genes involved in complex multicellular development in fungi and aid further studies on gene function and efforts to improve the productivity and heat tolerance in mushroom-forming fungi.
Additional Links: PMID-33064719
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@article {pmid33064719,
year = {2020},
author = {Liu, XB and Xia, EH and Li, M and Cui, YY and Wang, PM and Zhang, JX and Xie, BG and Xu, JP and Yan, JJ and Li, J and Nagy, LG and Yang, ZL},
title = {Transcriptome data reveal conserved patterns of fruiting body development and response to heat stress in the mushroom-forming fungus Flammulina filiformis.},
journal = {PloS one},
volume = {15},
number = {10},
pages = {e0239890},
pmid = {33064719},
issn = {1932-6203},
mesh = {Agaricales/*genetics/growth & development/metabolism ; Conserved Sequence ; *Evolution, Molecular ; Fruiting Bodies, Fungal/genetics/*growth & development/metabolism ; Fungal Proteins/genetics/metabolism ; Heat-Shock Proteins/genetics/metabolism ; *Heat-Shock Response ; *Transcriptome ; },
abstract = {Mushroom-forming fungi are complex multicellular organisms that form the basis of a large industry, yet, our understanding of the mechanisms of mushroom development and its responses to various stresses remains limited. The winter mushroom (Flammulina filiformis) is cultivated at a large commercial scale in East Asia and is a species with a preference for low temperatures. This study investigated fruiting body development in F. filiformis by comparing transcriptomes of 4 developmental stages, and compared the developmental genes to a 200-genome dataset to identify conserved genes involved in fruiting body development, and examined the response of heat sensitive and -resistant strains to heat stress. Our data revealed widely conserved genes involved in primordium development of F. filiformis, many of which originated before the emergence of the Agaricomycetes, indicating co-option for complex multicellularity during evolution. We also revealed several notable fruiting-specific genes, including the genes with conserved stipe-specific expression patterns and the others which related to sexual development, water absorption, basidium formation and sporulation, among others. Comparative analysis revealed that heat stress induced more genes in the heat resistant strain (M1) than in the heat sensitive one (XR). Of particular importance are the hsp70, hsp90 and fes1 genes, which may facilitate the adjustment to heat stress in the early stages of fruiting body development. These data highlighted novel genes involved in complex multicellular development in fungi and aid further studies on gene function and efforts to improve the productivity and heat tolerance in mushroom-forming fungi.},
}
MeSH Terms:
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Agaricales/*genetics/growth & development/metabolism
Conserved Sequence
*Evolution, Molecular
Fruiting Bodies, Fungal/genetics/*growth & development/metabolism
Fungal Proteins/genetics/metabolism
Heat-Shock Proteins/genetics/metabolism
*Heat-Shock Response
*Transcriptome
RevDate: 2020-11-13
Evolution of multicellularity by collective integration of spatial information.
eLife, 9:.
At the origin of multicellularity, cells may have evolved aggregation in response to predation, for functional specialisation or to allow large-scale integration of environmental cues. These group-level properties emerged from the interactions between cells in a group, and determined the selection pressures experienced by these cells. We investigate the evolution of multicellularity with an evolutionary model where cells search for resources by chemotaxis in a shallow, noisy gradient. Cells can evolve their adhesion to others in a periodically changing environment, where a cell's fitness solely depends on its distance from the gradient source. We show that multicellular aggregates evolve because they perform chemotaxis more efficiently than single cells. Only when the environment changes too frequently, a unicellular state evolves which relies on cell dispersal. Both strategies prevent the invasion of the other through interference competition, creating evolutionary bi-stability. Therefore, collective behaviour can be an emergent selective driver for undifferentiated multicellularity.
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@article {pmid33064078,
year = {2020},
author = {Colizzi, ES and Vroomans, RM and Merks, RM},
title = {Evolution of multicellularity by collective integration of spatial information.},
journal = {eLife},
volume = {9},
number = {},
pages = {},
pmid = {33064078},
issn = {2050-084X},
support = {StartImpuls//Nederlands Wetenschap Agenda/International ; 865.17.004//NWO/ENW-VICI/International ; Nederlands Wetenschap Agenda StartImpuls//Nederlandse Organisatie voor Wetenschappelijk Onderzoek/International ; NWO/ENW-VICI 865.17.004//Nederlandse Organisatie voor Wetenschappelijk Onderzoek/International ; },
abstract = {At the origin of multicellularity, cells may have evolved aggregation in response to predation, for functional specialisation or to allow large-scale integration of environmental cues. These group-level properties emerged from the interactions between cells in a group, and determined the selection pressures experienced by these cells. We investigate the evolution of multicellularity with an evolutionary model where cells search for resources by chemotaxis in a shallow, noisy gradient. Cells can evolve their adhesion to others in a periodically changing environment, where a cell's fitness solely depends on its distance from the gradient source. We show that multicellular aggregates evolve because they perform chemotaxis more efficiently than single cells. Only when the environment changes too frequently, a unicellular state evolves which relies on cell dispersal. Both strategies prevent the invasion of the other through interference competition, creating evolutionary bi-stability. Therefore, collective behaviour can be an emergent selective driver for undifferentiated multicellularity.},
}
RevDate: 2020-10-22
Interplay of mesoscale physics and agent-like behaviors in the parallel evolution of aggregative multicellularity.
EvoDevo, 11:21.
Myxobacteria and dictyostelids are prokaryotic and eukaryotic multicellular lineages, respectively, that after nutrient depletion aggregate and develop into structures called fruiting bodies. The developmental processes and resulting morphological outcomes resemble one another to a remarkable extent despite their independent origins, the evolutionary distance between them and the lack of traceable homology in molecular mechanisms. We hypothesize that the morphological parallelism between the two lineages arises as the consequence of the interplay within multicellular aggregates between generic processes, physical and physicochemical processes operating similarly in living and non-living matter at the mesoscale (~10-3-10-1 m) and agent-like behaviors, unique to living systems and characteristic of the constituent cells, considered as autonomous entities acting according to internal rules in a shared environment. Here, we analyze the contributions of generic and agent-like determinants in myxobacteria and dictyostelid development and their roles in the generation of their common traits. Consequent to aggregation, collective cell-cell contacts mediate the emergence of liquid-like properties, making nascent multicellular masses subject to novel patterning and morphogenetic processes. In both lineages, this leads to behaviors such as streaming, rippling, and rounding-up, as seen in non-living fluids. Later the aggregates solidify, leading them to exhibit additional generic properties and motifs. Computational models suggest that the morphological phenotypes of the multicellular masses deviate from the predictions of generic physics due to the contribution of agent-like behaviors of cells such as directed migration, quiescence, and oscillatory signal transduction mediated by responses to external cues. These employ signaling mechanisms that reflect the evolutionary histories of the respective organisms. We propose that the similar developmental trajectories of myxobacteria and dictyostelids are more due to shared generic physical processes in coordination with analogous agent-type behaviors than to convergent evolution under parallel selection regimes. Insights from the biology of these aggregative forms may enable a unified understanding of developmental evolution, including that of animals and plants.
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@article {pmid33062243,
year = {2020},
author = {Arias Del Angel, JA and Nanjundiah, V and Benítez, M and Newman, SA},
title = {Interplay of mesoscale physics and agent-like behaviors in the parallel evolution of aggregative multicellularity.},
journal = {EvoDevo},
volume = {11},
number = {},
pages = {21},
pmid = {33062243},
issn = {2041-9139},
abstract = {Myxobacteria and dictyostelids are prokaryotic and eukaryotic multicellular lineages, respectively, that after nutrient depletion aggregate and develop into structures called fruiting bodies. The developmental processes and resulting morphological outcomes resemble one another to a remarkable extent despite their independent origins, the evolutionary distance between them and the lack of traceable homology in molecular mechanisms. We hypothesize that the morphological parallelism between the two lineages arises as the consequence of the interplay within multicellular aggregates between generic processes, physical and physicochemical processes operating similarly in living and non-living matter at the mesoscale (~10-3-10-1 m) and agent-like behaviors, unique to living systems and characteristic of the constituent cells, considered as autonomous entities acting according to internal rules in a shared environment. Here, we analyze the contributions of generic and agent-like determinants in myxobacteria and dictyostelid development and their roles in the generation of their common traits. Consequent to aggregation, collective cell-cell contacts mediate the emergence of liquid-like properties, making nascent multicellular masses subject to novel patterning and morphogenetic processes. In both lineages, this leads to behaviors such as streaming, rippling, and rounding-up, as seen in non-living fluids. Later the aggregates solidify, leading them to exhibit additional generic properties and motifs. Computational models suggest that the morphological phenotypes of the multicellular masses deviate from the predictions of generic physics due to the contribution of agent-like behaviors of cells such as directed migration, quiescence, and oscillatory signal transduction mediated by responses to external cues. These employ signaling mechanisms that reflect the evolutionary histories of the respective organisms. We propose that the similar developmental trajectories of myxobacteria and dictyostelids are more due to shared generic physical processes in coordination with analogous agent-type behaviors than to convergent evolution under parallel selection regimes. Insights from the biology of these aggregative forms may enable a unified understanding of developmental evolution, including that of animals and plants.},
}
RevDate: 2020-10-27
CmpDate: 2020-10-27
Engineering synthetic morphogen systems that can program multicellular patterning.
Science (New York, N.Y.), 370(6514):327-331.
In metazoan tissues, cells decide their fates by sensing positional information provided by specialized morphogen proteins. To explore what features are sufficient for positional encoding, we asked whether arbitrary molecules (e.g., green fluorescent protein or mCherry) could be converted into synthetic morphogens. Synthetic morphogens expressed from a localized source formed a gradient when trapped by surface-anchoring proteins, and they could be sensed by synthetic receptors. Despite their simplicity, these morphogen systems yielded patterns reminiscent of those observed in vivo. Gradients could be reshaped by altering anchor density or by providing a source of competing inhibitor. Gradient interpretation could be altered by adding feedback loops or morphogen cascades to receiver cell response circuits. Orthogonal cell-cell communication systems provide insight into morphogen evolution and a platform for engineering tissues.
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@article {pmid33060357,
year = {2020},
author = {Toda, S and McKeithan, WL and Hakkinen, TJ and Lopez, P and Klein, OD and Lim, WA},
title = {Engineering synthetic morphogen systems that can program multicellular patterning.},
journal = {Science (New York, N.Y.)},
volume = {370},
number = {6514},
pages = {327-331},
doi = {10.1126/science.abc0033},
pmid = {33060357},
issn = {1095-9203},
support = {F32 DK123939/DK/NIDDK NIH HHS/United States ; R01 DE028496/DE/NIDCR NIH HHS/United States ; R35 DE026602/DE/NIDCR NIH HHS/United States ; /HHMI/Howard Hughes Medical Institute/United States ; },
mesh = {Animals ; *Body Patterning ; Drosophila melanogaster/growth & development ; Fibroblasts ; Green Fluorescent Proteins/genetics/*metabolism ; Protein Engineering ; Receptors, Notch/genetics/metabolism ; Tissue Engineering/*methods ; },
abstract = {In metazoan tissues, cells decide their fates by sensing positional information provided by specialized morphogen proteins. To explore what features are sufficient for positional encoding, we asked whether arbitrary molecules (e.g., green fluorescent protein or mCherry) could be converted into synthetic morphogens. Synthetic morphogens expressed from a localized source formed a gradient when trapped by surface-anchoring proteins, and they could be sensed by synthetic receptors. Despite their simplicity, these morphogen systems yielded patterns reminiscent of those observed in vivo. Gradients could be reshaped by altering anchor density or by providing a source of competing inhibitor. Gradient interpretation could be altered by adding feedback loops or morphogen cascades to receiver cell response circuits. Orthogonal cell-cell communication systems provide insight into morphogen evolution and a platform for engineering tissues.},
}
MeSH Terms:
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Animals
*Body Patterning
Drosophila melanogaster/growth & development
Fibroblasts
Green Fluorescent Proteins/genetics/*metabolism
Protein Engineering
Receptors, Notch/genetics/metabolism
Tissue Engineering/*methods
RevDate: 2020-10-28
Damage Repair versus Aging in an Individual-Based Model of Biofilms.
mSystems, 5(5):.
The extent of senescence due to damage accumulation-or aging-is evidently evolvable as it differs hugely between species and is not universal, suggesting that its fitness advantages depend on life history and environment. In contrast, repair of damage is present in all organisms studied. Despite the fundamental trade-off between investing resources into repair or into growth, repair and segregation of damage have not always been considered alternatives. For unicellular organisms, unrepaired damage could be divided asymmetrically between daughter cells, leading to senescence of one and rejuvenation of the other. Repair of "unicells" has been predicted to be advantageous in well-mixed environments such as chemostats. Most microorganisms, however, live in spatially structured systems, such as biofilms, with gradients of environmental conditions and cellular physiology as well as a clonal population structure. To investigate whether this clonal structure might favor senescence by damage segregation (a division-of-labor strategy akin to the germline-soma division in multicellular organisms), we used an individual-based computational model and developed an adaptive repair strategy where cells respond to their current intracellular damage levels by investing into repair machinery accordingly. Our simulations showed that the new adaptive repair strategy was advantageous provided that growth was limited by substrate availability, which is typical for biofilms. Thus, biofilms do not favor a germline-soma-like division of labor between daughter cells in terms of damage segregation. We suggest that damage segregation is beneficial only when extrinsic mortality is high, a degree of multicellularity is present, and an active mechanism makes segregation effective.IMPORTANCE Damage is an inevitable consequence of life. For unicellular organisms, this leads to a trade-off between allocating resources into damage repair or into growth coupled with segregation of damage upon cell division, i.e., aging and senescence. Few studies considered repair as an alternative to senescence. None considered biofilms, where the majority of unicellular organisms live, although fitness advantages in well-mixed systems often turn into disadvantages in spatially structured systems such as biofilms. We compared the fitness consequences of aging versus an adaptive repair mechanism based on sensing damage, using an individual-based model of a generic unicellular organism growing in biofilms. We found that senescence is not beneficial provided that growth is limited by substrate availability. Instead, it is useful as a stress response to deal with damage that failed to be repaired when (i) extrinsic mortality was high; (ii) a degree of multicellularity was present; and (iii) damage segregation was effective.
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@article {pmid33051374,
year = {2020},
author = {Wright, RJ and Clegg, RJ and Coker, TLR and Kreft, JU},
title = {Damage Repair versus Aging in an Individual-Based Model of Biofilms.},
journal = {mSystems},
volume = {5},
number = {5},
pages = {},
pmid = {33051374},
issn = {2379-5077},
abstract = {The extent of senescence due to damage accumulation-or aging-is evidently evolvable as it differs hugely between species and is not universal, suggesting that its fitness advantages depend on life history and environment. In contrast, repair of damage is present in all organisms studied. Despite the fundamental trade-off between investing resources into repair or into growth, repair and segregation of damage have not always been considered alternatives. For unicellular organisms, unrepaired damage could be divided asymmetrically between daughter cells, leading to senescence of one and rejuvenation of the other. Repair of "unicells" has been predicted to be advantageous in well-mixed environments such as chemostats. Most microorganisms, however, live in spatially structured systems, such as biofilms, with gradients of environmental conditions and cellular physiology as well as a clonal population structure. To investigate whether this clonal structure might favor senescence by damage segregation (a division-of-labor strategy akin to the germline-soma division in multicellular organisms), we used an individual-based computational model and developed an adaptive repair strategy where cells respond to their current intracellular damage levels by investing into repair machinery accordingly. Our simulations showed that the new adaptive repair strategy was advantageous provided that growth was limited by substrate availability, which is typical for biofilms. Thus, biofilms do not favor a germline-soma-like division of labor between daughter cells in terms of damage segregation. We suggest that damage segregation is beneficial only when extrinsic mortality is high, a degree of multicellularity is present, and an active mechanism makes segregation effective.IMPORTANCE Damage is an inevitable consequence of life. For unicellular organisms, this leads to a trade-off between allocating resources into damage repair or into growth coupled with segregation of damage upon cell division, i.e., aging and senescence. Few studies considered repair as an alternative to senescence. None considered biofilms, where the majority of unicellular organisms live, although fitness advantages in well-mixed systems often turn into disadvantages in spatially structured systems such as biofilms. We compared the fitness consequences of aging versus an adaptive repair mechanism based on sensing damage, using an individual-based model of a generic unicellular organism growing in biofilms. We found that senescence is not beneficial provided that growth is limited by substrate availability. Instead, it is useful as a stress response to deal with damage that failed to be repaired when (i) extrinsic mortality was high; (ii) a degree of multicellularity was present; and (iii) damage segregation was effective.},
}
RevDate: 2020-11-10
Diversity of GPI-anchored fungal adhesins.
Biological chemistry, 401(12):1389-1405.
Selective adhesion of fungal cells to one another and to foreign surfaces is fundamental for the development of multicellular growth forms and the successful colonization of substrates and host organisms. Accordingly, fungi possess diverse cell wall-associated adhesins, mostly large glycoproteins, which present N-terminal adhesion domains at the cell surface for ligand recognition and binding. In order to function as robust adhesins, these glycoproteins must be covalently linkedto the cell wall via C-terminal glycosylphosphatidylinositol (GPI) anchors by transglycosylation. In this review, we summarize the current knowledge on the structural and functional diversity of so far characterized protein families of adhesion domains and set it into a broad context by an in-depth bioinformatics analysis using sequence similarity networks. In addition, we discuss possible mechanisms for the membrane-to-cell wall transfer of fungal adhesins by membrane-anchored Dfg5 transglycosidases.
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@article {pmid33035180,
year = {2020},
author = {Essen, LO and Vogt, MS and Mösch, HU},
title = {Diversity of GPI-anchored fungal adhesins.},
journal = {Biological chemistry},
volume = {401},
number = {12},
pages = {1389-1405},
doi = {10.1515/hsz-2020-0199},
pmid = {33035180},
issn = {1437-4315},
abstract = {Selective adhesion of fungal cells to one another and to foreign surfaces is fundamental for the development of multicellular growth forms and the successful colonization of substrates and host organisms. Accordingly, fungi possess diverse cell wall-associated adhesins, mostly large glycoproteins, which present N-terminal adhesion domains at the cell surface for ligand recognition and binding. In order to function as robust adhesins, these glycoproteins must be covalently linkedto the cell wall via C-terminal glycosylphosphatidylinositol (GPI) anchors by transglycosylation. In this review, we summarize the current knowledge on the structural and functional diversity of so far characterized protein families of adhesion domains and set it into a broad context by an in-depth bioinformatics analysis using sequence similarity networks. In addition, we discuss possible mechanisms for the membrane-to-cell wall transfer of fungal adhesins by membrane-anchored Dfg5 transglycosidases.},
}
RevDate: 2020-10-19
Tracking the evolutionary innovations of plant terrestrialization.
Gene pii:S0378-1119(20)30872-6 [Epub ahead of print].
The gradual transition of the algal ancestor from the freshwater to land has always attracted evolutionary biologists. The recent report of high-quality reference genomes of five Charophyta algae (Spirogloea muscicola, Mesotaenium endlicherianum, Mesostigma viride, Chlorokybus atmophyticus and Penium margaritaceum) and one hornwort (Anthoceros angustus) species sheds light on this fascinating transition. These early diverging plants and algae could have gained new genes from soil bacteria and fungi through horizontal gene transfer (HGT), which was so common during plant terrestrialization and may outrun our expectations. Through reviewing and critical thinking about the advancements on these plant genomes, here, I propose three prospective research directions that need to address in the future: (i) due to the ubiquitous nature of viruses that is similar to soil bacteria and fungi, there is less attention to viruses that probably also play an important role in the genome evolution of plants via HGT; (ii) multicellularity has occurred many times independently, but we still know a little about the biological and ecological mechanisms leading to multi-cellularity in Streptophyta; (iii) and most importantly, the quantitative relationships between genetic innovations and environmental variables such as temperature, precipitation and solar radiation, need pioneering research collaborated by biological evolutionists, computer scientists, and ecologists, which are crucial for understanding the macroevolution of plants and could also be used to simulate the evolution of plants under future climate change.
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PubMed:
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@article {pmid33031891,
year = {2020},
author = {Gao, JG},
title = {Tracking the evolutionary innovations of plant terrestrialization.},
journal = {Gene},
volume = {},
number = {},
pages = {145203},
doi = {10.1016/j.gene.2020.145203},
pmid = {33031891},
issn = {1879-0038},
abstract = {The gradual transition of the algal ancestor from the freshwater to land has always attracted evolutionary biologists. The recent report of high-quality reference genomes of five Charophyta algae (Spirogloea muscicola, Mesotaenium endlicherianum, Mesostigma viride, Chlorokybus atmophyticus and Penium margaritaceum) and one hornwort (Anthoceros angustus) species sheds light on this fascinating transition. These early diverging plants and algae could have gained new genes from soil bacteria and fungi through horizontal gene transfer (HGT), which was so common during plant terrestrialization and may outrun our expectations. Through reviewing and critical thinking about the advancements on these plant genomes, here, I propose three prospective research directions that need to address in the future: (i) due to the ubiquitous nature of viruses that is similar to soil bacteria and fungi, there is less attention to viruses that probably also play an important role in the genome evolution of plants via HGT; (ii) multicellularity has occurred many times independently, but we still know a little about the biological and ecological mechanisms leading to multi-cellularity in Streptophyta; (iii) and most importantly, the quantitative relationships between genetic innovations and environmental variables such as temperature, precipitation and solar radiation, need pioneering research collaborated by biological evolutionists, computer scientists, and ecologists, which are crucial for understanding the macroevolution of plants and could also be used to simulate the evolution of plants under future climate change.},
}
RevDate: 2020-10-10
The algal selenoproteomes.
BMC genomics, 21(1):699.
BACKGROUND: Selenium is an essential trace element, and selenocysteine (Sec, U) is its predominant form in vivo. Proteins that contain Sec are selenoproteins, whose special structural features include not only the TGA codon encoding Sec but also the SECIS element in mRNA and the conservation of the Sec-flanking region. These unique features have led to the development of a series of bioinformatics methods to predict and research selenoprotein genes. There have been some studies and reports on the evolution and distribution of selenoprotein genes in prokaryotes and multicellular eukaryotes, but the systematic analysis of single-cell eukaryotes, especially algae, has been very limited.
RESULTS: In this study, we predicted selenoprotein genes in 137 species of algae by using a program we previously developed. More than 1000 selenoprotein genes were obtained. A database website was built to record these algae selenoprotein genes (www.selenoprotein.com). These genes belong to 42 selenoprotein families, including three novel selenoprotein gene families.
CONCLUSIONS: This study reveals the primordial state of the eukaryotic selenoproteome. It is an important clue to explore the significance of selenium for primordial eukaryotes and to determine the complete evolutionary spectrum of selenoproteins in all life forms.
Additional Links: PMID-33028229
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@article {pmid33028229,
year = {2020},
author = {Jiang, L and Lu, Y and Zheng, L and Li, G and Chen, L and Zhang, M and Ni, J and Liu, Q and Zhang, Y},
title = {The algal selenoproteomes.},
journal = {BMC genomics},
volume = {21},
number = {1},
pages = {699},
pmid = {33028229},
issn = {1471-2164},
support = {31401129//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: Selenium is an essential trace element, and selenocysteine (Sec, U) is its predominant form in vivo. Proteins that contain Sec are selenoproteins, whose special structural features include not only the TGA codon encoding Sec but also the SECIS element in mRNA and the conservation of the Sec-flanking region. These unique features have led to the development of a series of bioinformatics methods to predict and research selenoprotein genes. There have been some studies and reports on the evolution and distribution of selenoprotein genes in prokaryotes and multicellular eukaryotes, but the systematic analysis of single-cell eukaryotes, especially algae, has been very limited.
RESULTS: In this study, we predicted selenoprotein genes in 137 species of algae by using a program we previously developed. More than 1000 selenoprotein genes were obtained. A database website was built to record these algae selenoprotein genes (www.selenoprotein.com). These genes belong to 42 selenoprotein families, including three novel selenoprotein gene families.
CONCLUSIONS: This study reveals the primordial state of the eukaryotic selenoproteome. It is an important clue to explore the significance of selenium for primordial eukaryotes and to determine the complete evolutionary spectrum of selenoproteins in all life forms.},
}
RevDate: 2020-10-07
Artificial selection for host resistance to tumour growth and subsequent cancer cell adaptations: an evolutionary arms race.
British journal of cancer pii:10.1038/s41416-020-01110-1 [Epub ahead of print].
BACKGROUND: Cancer progression is governed by evolutionary dynamics in both the tumour population and its host. Since cancers die with the host, each new population of cancer cells must reinvent strategies to overcome the host's heritable defences. In contrast, host species evolve defence strategies over generations if tumour development limits procreation.
METHODS: We investigate this "evolutionary arms race" through intentional breeding of immunodeficient SCID and immunocompetent Black/6 mice to evolve increased tumour suppression. Over 10 generations, we injected Lewis lung mouse carcinoma cells [LL/2-Luc-M38] and selectively bred the two individuals with the slowest tumour growth at day 11. Their male progeny were hosts in the subsequent round.
RESULTS: The evolved SCID mice suppressed tumour growth through biomechanical restriction from increased mesenchymal proliferation, and the evolved Black/6 mice suppressed tumour growth by increasing immune-mediated killing of cancer cells. However, transcriptomic changes of multicellular tissue organisation and function genes allowed LL/2-Luc-M38 cells to adapt through increased matrix remodelling in SCID mice, and reduced angiogenesis, increased energy utilisation and accelerated proliferation in Black/6 mice.
CONCLUSION: Host species can rapidly evolve both immunologic and non-immunologic tumour defences. However, cancer cell plasticity allows effective phenotypic and population-based counter strategies.
Additional Links: PMID-33024265
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@article {pmid33024265,
year = {2020},
author = {Ibrahim-Hashim, A and Luddy, K and Abrahams, D and Enriquez-Navas, P and Damgaci, S and Yao, J and Chen, T and Bui, MM and Gillies, RJ and O'Farrelly, C and Richards, CL and Brown, JS and Gatenby, RA},
title = {Artificial selection for host resistance to tumour growth and subsequent cancer cell adaptations: an evolutionary arms race.},
journal = {British journal of cancer},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41416-020-01110-1},
pmid = {33024265},
issn = {1532-1827},
support = {P30-CA076292//U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)/ ; U54 CA143970/CA/NCI NIH HHS/United States ; P30-CA076292//U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)/ ; U54 CA143970/CA/NCI NIH HHS/United States ; P30-CA076292//U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)/ ; U54 CA143970/CA/NCI NIH HHS/United States ; R01 CA077575/CA/NCI NIH HHS/United States ; P30-CA076292//U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)/ ; },
abstract = {BACKGROUND: Cancer progression is governed by evolutionary dynamics in both the tumour population and its host. Since cancers die with the host, each new population of cancer cells must reinvent strategies to overcome the host's heritable defences. In contrast, host species evolve defence strategies over generations if tumour development limits procreation.
METHODS: We investigate this "evolutionary arms race" through intentional breeding of immunodeficient SCID and immunocompetent Black/6 mice to evolve increased tumour suppression. Over 10 generations, we injected Lewis lung mouse carcinoma cells [LL/2-Luc-M38] and selectively bred the two individuals with the slowest tumour growth at day 11. Their male progeny were hosts in the subsequent round.
RESULTS: The evolved SCID mice suppressed tumour growth through biomechanical restriction from increased mesenchymal proliferation, and the evolved Black/6 mice suppressed tumour growth by increasing immune-mediated killing of cancer cells. However, transcriptomic changes of multicellular tissue organisation and function genes allowed LL/2-Luc-M38 cells to adapt through increased matrix remodelling in SCID mice, and reduced angiogenesis, increased energy utilisation and accelerated proliferation in Black/6 mice.
CONCLUSION: Host species can rapidly evolve both immunologic and non-immunologic tumour defences. However, cancer cell plasticity allows effective phenotypic and population-based counter strategies.},
}
RevDate: 2020-10-06
Comparative genomics and pan-genomics of the Myxococcaceae, including a description of five novel species: Myxococcus eversor sp. nov., Myxococcus llanfairpwllgwyngyllgogerychwyrndrobwllllantysiliogogogochensis sp. nov., Myxococcus vastator sp. nov., Pyxidicoccus caerfyrddinensis sp. nov. and Pyxidicoccus trucidator sp. nov.
Genome biology and evolution pii:5918458 [Epub ahead of print].
Members of the predatory Myxococcales (myxobacteria) possess large genomes, undergo multicellular development and produce diverse secondary metabolites, which are being actively prospected for novel drug discovery. To direct such efforts, it is important to understand the relationships between myxobacterial ecology, evolution, taxonomy and genomic variation. This study investigated the genomes and pan-genomes of organisms within the Myxococcaceae, including the genera Myxococcus and Corallococcus, the most abundant myxobacteria isolated from soils. Previously, ten species of Corallococcus were known, while six species of Myxococcus phylogenetically surrounded a third genus (Pyxidicoccus) composed of a single species. Here, we describe draft genome sequences of five novel species within the Myxococcaceae (Myxococcus eversor, Myxococcus llanfairpwllgwyngyllgogerychwyrndrobwllllantysiliogogogochensis, Myxococcus vastator, Pyxidicoccus caerfyrddinensis and Pyxidicoccus trucidator), and for the Pyxidicoccus type species strain, Pyxidicoccus fallax DSM 14698T. Genomic and physiological comparisons demonstrated clear differences between the five novel species and every other Myxococcus or Pyxidicoccus spp. type strain. Subsequent analyses of type strain genomes showed that both the Corallococcus pan-genome and the combined Myxococcus and Pyxidicoccus (Myxococcus/Pyxidicoccus) pan-genome are large and open, but with clear differences. Genomes of Corallococcus spp. are generally smaller than those of Myxococcus/Pyxidicoccus spp., but have core genomes three times larger. Myxococcus/Pyxidicoccus spp. genomes are more variable in size, with larger and more unique sets of accessory genes than those of Corallococcus species. In both genera, biosynthetic gene clusters are relatively enriched in the shell pan-genomes, implying they grant a greater evolutionary benefit than other shell genes, presumably by conferring selective advantages during predation.
Additional Links: PMID-33022031
Publisher:
PubMed:
Citation:
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@article {pmid33022031,
year = {2020},
author = {Chambers, J and Sparks, N and Sydney, N and Livingstone, PG and Cookson, AR and Whitworth, DE},
title = {Comparative genomics and pan-genomics of the Myxococcaceae, including a description of five novel species: Myxococcus eversor sp. nov., Myxococcus llanfairpwllgwyngyllgogerychwyrndrobwllllantysiliogogogochensis sp. nov., Myxococcus vastator sp. nov., Pyxidicoccus caerfyrddinensis sp. nov. and Pyxidicoccus trucidator sp. nov.},
journal = {Genome biology and evolution},
volume = {},
number = {},
pages = {},
doi = {10.1093/gbe/evaa212},
pmid = {33022031},
issn = {1759-6653},
abstract = {Members of the predatory Myxococcales (myxobacteria) possess large genomes, undergo multicellular development and produce diverse secondary metabolites, which are being actively prospected for novel drug discovery. To direct such efforts, it is important to understand the relationships between myxobacterial ecology, evolution, taxonomy and genomic variation. This study investigated the genomes and pan-genomes of organisms within the Myxococcaceae, including the genera Myxococcus and Corallococcus, the most abundant myxobacteria isolated from soils. Previously, ten species of Corallococcus were known, while six species of Myxococcus phylogenetically surrounded a third genus (Pyxidicoccus) composed of a single species. Here, we describe draft genome sequences of five novel species within the Myxococcaceae (Myxococcus eversor, Myxococcus llanfairpwllgwyngyllgogerychwyrndrobwllllantysiliogogogochensis, Myxococcus vastator, Pyxidicoccus caerfyrddinensis and Pyxidicoccus trucidator), and for the Pyxidicoccus type species strain, Pyxidicoccus fallax DSM 14698T. Genomic and physiological comparisons demonstrated clear differences between the five novel species and every other Myxococcus or Pyxidicoccus spp. type strain. Subsequent analyses of type strain genomes showed that both the Corallococcus pan-genome and the combined Myxococcus and Pyxidicoccus (Myxococcus/Pyxidicoccus) pan-genome are large and open, but with clear differences. Genomes of Corallococcus spp. are generally smaller than those of Myxococcus/Pyxidicoccus spp., but have core genomes three times larger. Myxococcus/Pyxidicoccus spp. genomes are more variable in size, with larger and more unique sets of accessory genes than those of Corallococcus species. In both genera, biosynthetic gene clusters are relatively enriched in the shell pan-genomes, implying they grant a greater evolutionary benefit than other shell genes, presumably by conferring selective advantages during predation.},
}
RevDate: 2020-10-20
Deep phylogeny of cancer drivers and compensatory mutations.
Communications biology, 3(1):551.
Driver mutations (DM) are the genetic impetus for most cancers. The DM are assumed to be deleterious in species evolution, being eliminated by purifying selection unless compensated by other mutations. We present deep phylogenies for 84 cancer driver genes and investigate the prevalence of 434 DM across gene-species trees. The DM are rare in species evolution, and 181 are completely absent, validating their negative fitness effect. The DM are more common in unicellular than in multicellular eukaryotes, suggesting a link between these mutations and cell proliferation control. 18 DM appear as the ancestral state in one or more major clades, including 3 among mammals. We identify within-gene, compensatory mutations for 98 DM and infer likely interactions between the DM and compensatory sites in protein structures. These findings elucidate the evolutionary status of DM and are expected to advance the understanding of the functions and evolution of oncogenes and tumor suppressors.
Additional Links: PMID-33009502
PubMed:
Citation:
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@article {pmid33009502,
year = {2020},
author = {Rochman, ND and Wolf, YI and Koonin, EV},
title = {Deep phylogeny of cancer drivers and compensatory mutations.},
journal = {Communications biology},
volume = {3},
number = {1},
pages = {551},
pmid = {33009502},
issn = {2399-3642},
abstract = {Driver mutations (DM) are the genetic impetus for most cancers. The DM are assumed to be deleterious in species evolution, being eliminated by purifying selection unless compensated by other mutations. We present deep phylogenies for 84 cancer driver genes and investigate the prevalence of 434 DM across gene-species trees. The DM are rare in species evolution, and 181 are completely absent, validating their negative fitness effect. The DM are more common in unicellular than in multicellular eukaryotes, suggesting a link between these mutations and cell proliferation control. 18 DM appear as the ancestral state in one or more major clades, including 3 among mammals. We identify within-gene, compensatory mutations for 98 DM and infer likely interactions between the DM and compensatory sites in protein structures. These findings elucidate the evolutionary status of DM and are expected to advance the understanding of the functions and evolution of oncogenes and tumor suppressors.},
}
RevDate: 2020-10-02
The Curious Strategy of Multipartite Viruses.
Annual review of virology, 7(1):203-218.
Multipartite virus genomes are composed of several segments, each packaged in a distinct viral particle. Although this puzzling genome architecture is found in ∼17% of known viral species, its distribution among hosts or among distinct types of genome-composing nucleic acid remains poorly understood. No convincing advantage of multipartitism has been identified, yet the maintenance of genomic integrity appears problematic. Here we review recent studies shedding light on these issues. Multipartite viruses rapidly modify the copy number of each segment/gene from one host species to another, a putative benefit if host switches are common. One multipartite virus functions in a multicellular way: The segments do not all need to be present in the same cell and can functionally complement across cells, maintaining genome integrity within hosts. The genomic integrity maintenance during host-to-host transmission needs further elucidation. These features challenge several virology foundations and could apply to other multicomponent viral systems.
Additional Links: PMID-32991271
Publisher:
PubMed:
Citation:
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@article {pmid32991271,
year = {2020},
author = {Michalakis, Y and Blanc, S},
title = {The Curious Strategy of Multipartite Viruses.},
journal = {Annual review of virology},
volume = {7},
number = {1},
pages = {203-218},
doi = {10.1146/annurev-virology-010220-063346},
pmid = {32991271},
issn = {2327-0578},
abstract = {Multipartite virus genomes are composed of several segments, each packaged in a distinct viral particle. Although this puzzling genome architecture is found in ∼17% of known viral species, its distribution among hosts or among distinct types of genome-composing nucleic acid remains poorly understood. No convincing advantage of multipartitism has been identified, yet the maintenance of genomic integrity appears problematic. Here we review recent studies shedding light on these issues. Multipartite viruses rapidly modify the copy number of each segment/gene from one host species to another, a putative benefit if host switches are common. One multipartite virus functions in a multicellular way: The segments do not all need to be present in the same cell and can functionally complement across cells, maintaining genome integrity within hosts. The genomic integrity maintenance during host-to-host transmission needs further elucidation. These features challenge several virology foundations and could apply to other multicomponent viral systems.},
}
RevDate: 2020-10-10
Diverse phylogeny and morphology of magnetite biomineralized by magnetotactic cocci.
Environmental microbiology [Epub ahead of print].
Magnetotactic bacteria (MTB) are diverse prokaryotes that produce magnetic nanocrystals within intracellular membranes (magnetosomes). Here, we present a large-scale analysis of diversity and magnetosome biomineralization in modern magnetotactic cocci, which are the most abundant MTB morphotypes in nature. Nineteen novel magnetotactic cocci species are identified phylogenetically and structurally at the single-cell level. Phylogenetic analysis demonstrates that the cocci cluster into an independent branch from other Alphaproteobacteria MTB, that is, within the Etaproteobacteria class in the Proteobacteria phylum. Statistical analysis reveals species-specific biomineralization of magnetosomal magnetite morphologies. This further confirms that magnetosome biomineralization is controlled strictly by the MTB cell and differs among species or strains. The post-mortem remains of MTB are often preserved as magnetofossils within sediments or sedimentary rocks, yet paleobiological and geological interpretation of their fossil record remains challenging. Our results indicate that magnetofossil morphology could be a promising proxy for retrieving paleobiological information about ancient MTB.
Additional Links: PMID-32985765
Publisher:
PubMed:
Citation:
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@article {pmid32985765,
year = {2020},
author = {Liu, P and Liu, Y and Zhao, X and Roberts, AP and Zhang, H and Zheng, Y and Wang, F and Wang, L and Menguy, N and Pan, Y and Li, J},
title = {Diverse phylogeny and morphology of magnetite biomineralized by magnetotactic cocci.},
journal = {Environmental microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1111/1462-2920.15254},
pmid = {32985765},
issn = {1462-2920},
support = {MGQNLM201704//Laboratory for Marine Geology, Qingdao National Laboratory for Marine Science and Technology/ ; 41621004//National Natural Science Foundation of China/ ; 41890843//National Natural Science Foundation of China/ ; 41920104009//National Natural Science Foundation of China/ ; RVKEXUE2019GZ06//The Senior User Project of RVKEXUE2019GZ06 (Center for Ocean Mega-Science, Chinese Academy of Sciences)/ ; DP200100765//Australian Research Council/ ; DP140104544//Australian Research Council/ ; },
abstract = {Magnetotactic bacteria (MTB) are diverse prokaryotes that produce magnetic nanocrystals within intracellular membranes (magnetosomes). Here, we present a large-scale analysis of diversity and magnetosome biomineralization in modern magnetotactic cocci, which are the most abundant MTB morphotypes in nature. Nineteen novel magnetotactic cocci species are identified phylogenetically and structurally at the single-cell level. Phylogenetic analysis demonstrates that the cocci cluster into an independent branch from other Alphaproteobacteria MTB, that is, within the Etaproteobacteria class in the Proteobacteria phylum. Statistical analysis reveals species-specific biomineralization of magnetosomal magnetite morphologies. This further confirms that magnetosome biomineralization is controlled strictly by the MTB cell and differs among species or strains. The post-mortem remains of MTB are often preserved as magnetofossils within sediments or sedimentary rocks, yet paleobiological and geological interpretation of their fossil record remains challenging. Our results indicate that magnetofossil morphology could be a promising proxy for retrieving paleobiological information about ancient MTB.},
}
RevDate: 2020-10-01
Structure and Functions of Sidekicks.
Frontiers in molecular neuroscience, 13:139.
Many of the immunoglobulin superfamily (IgSF) molecules play pivotal roles in cell communication. The Sidekick (Sdk) gene, first described in Drosophila, encodes the single-pass transmembrane protein, Sdk, which is one of the largest among IgSF membrane proteins. Sdk first appeared in multicellular animals during the Precambrian age and later evolved to Sdk1 and Sdk2 in vertebrates by gene duplication. In flies, a single Sdk is involved in positioning photoreceptor neurons and their axons in the visual system and is responsible for dynamically rearranging cell shapes by strictly populating tricellular adherens junctions in epithelia. In vertebrates, Sdk1 and Sdk2 are expressed by unique sets of cell types and distinctively participate in the formation and/or maintenance of neural circuits in the retina, indicating that they are determinants of synaptic specificity. These functions are mediated by specific homophilic binding of their ectodomains and by intracellular association with PDZ scaffold proteins. Recent human genetic studies as well as animal experiments implicate that Sdk genes may influence various neurodevelopmental and psychiatric disorders, such as autism spectrum disorders, attention-deficit hyperactivity disorder, addiction, and depression. The gigantic Sdk1 gene is susceptible to erratic gene rearrangements or mutations in both somatic and germ-line cells, potentially contributing to neurological disorders and some types of cancers. This review summarizes what is known about the structure and roles of Sdks.
Additional Links: PMID-32982686
PubMed:
Citation:
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@article {pmid32982686,
year = {2020},
author = {Yamagata, M},
title = {Structure and Functions of Sidekicks.},
journal = {Frontiers in molecular neuroscience},
volume = {13},
number = {},
pages = {139},
pmid = {32982686},
issn = {1662-5099},
abstract = {Many of the immunoglobulin superfamily (IgSF) molecules play pivotal roles in cell communication. The Sidekick (Sdk) gene, first described in Drosophila, encodes the single-pass transmembrane protein, Sdk, which is one of the largest among IgSF membrane proteins. Sdk first appeared in multicellular animals during the Precambrian age and later evolved to Sdk1 and Sdk2 in vertebrates by gene duplication. In flies, a single Sdk is involved in positioning photoreceptor neurons and their axons in the visual system and is responsible for dynamically rearranging cell shapes by strictly populating tricellular adherens junctions in epithelia. In vertebrates, Sdk1 and Sdk2 are expressed by unique sets of cell types and distinctively participate in the formation and/or maintenance of neural circuits in the retina, indicating that they are determinants of synaptic specificity. These functions are mediated by specific homophilic binding of their ectodomains and by intracellular association with PDZ scaffold proteins. Recent human genetic studies as well as animal experiments implicate that Sdk genes may influence various neurodevelopmental and psychiatric disorders, such as autism spectrum disorders, attention-deficit hyperactivity disorder, addiction, and depression. The gigantic Sdk1 gene is susceptible to erratic gene rearrangements or mutations in both somatic and germ-line cells, potentially contributing to neurological disorders and some types of cancers. This review summarizes what is known about the structure and roles of Sdks.},
}
RevDate: 2020-09-25
Cooperation and Cheating among Germinating Spores.
Current biology : CB pii:S0960-9822(20)31281-1 [Epub ahead of print].
Many microbes produce stress-resistant spores to survive unfavorable conditions [1-4] and enhance dispersal [1, 5]. Cooperative behavior is integral to the process of spore formation in some species [3, 6], but the degree to which germination of spore populations involves social interactions remains little explored. Myxococcus xanthus is a predatory soil bacterium that upon starvation forms spore-filled multicellular fruiting bodies that often harbor substantial diversity of endemic origin [7, 8]. Here we demonstrate that germination of M. xanthus spores formed during fruiting-body development is a social process involving at least two functionally distinct social molecules. Using pairs of natural isolates each derived from a single fruiting body that emerged on soil, we first show that spore germination exhibits positive density dependence due to a secreted "public-good" germination factor. Further, we find that a germination defect of one strain under saline stress in pure culture is complemented by addition of another strain that germinates well in saline environments and mediates cheating by the defective strain. Glycine betaine, an osmo-protectant utilized in all domains of life, is found to mediate saline-specific density dependence and cheating. Density dependence in non-saline conditions is mediated by a distinct factor, revealing socially complex spore germination involving multiple social molecules.
Additional Links: PMID-32976811
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PubMed:
Citation:
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@article {pmid32976811,
year = {2020},
author = {Pande, S and Pérez Escriva, P and Yu, YN and Sauer, U and Velicer, GJ},
title = {Cooperation and Cheating among Germinating Spores.},
journal = {Current biology : CB},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cub.2020.08.091},
pmid = {32976811},
issn = {1879-0445},
abstract = {Many microbes produce stress-resistant spores to survive unfavorable conditions [1-4] and enhance dispersal [1, 5]. Cooperative behavior is integral to the process of spore formation in some species [3, 6], but the degree to which germination of spore populations involves social interactions remains little explored. Myxococcus xanthus is a predatory soil bacterium that upon starvation forms spore-filled multicellular fruiting bodies that often harbor substantial diversity of endemic origin [7, 8]. Here we demonstrate that germination of M. xanthus spores formed during fruiting-body development is a social process involving at least two functionally distinct social molecules. Using pairs of natural isolates each derived from a single fruiting body that emerged on soil, we first show that spore germination exhibits positive density dependence due to a secreted "public-good" germination factor. Further, we find that a germination defect of one strain under saline stress in pure culture is complemented by addition of another strain that germinates well in saline environments and mediates cheating by the defective strain. Glycine betaine, an osmo-protectant utilized in all domains of life, is found to mediate saline-specific density dependence and cheating. Density dependence in non-saline conditions is mediated by a distinct factor, revealing socially complex spore germination involving multiple social molecules.},
}
RevDate: 2020-09-26
Toward the Discovery of Host-Defense Peptides in Plants.
Frontiers in immunology, 11:1825.
Defense peptides protect multicellular eukaryotes from infections. In biomedical sciences, a dominant conceptual framework refers to defense peptides as host-defense peptides (HDPs), which are bifunctional peptides with both direct antimicrobial and immunomodulatory activities. No HDP has been reported in plants so far, and the very concept of HDP has not been captured yet by the plant science community. Plant science thus lacks the conceptual framework that would coordinate research efforts aimed at discovering plant HDPs. In this perspective article, I used bibliometric and literature survey approaches to raise awareness about the HDP concept among plant scientists, and to encourage research efforts aimed at discovering plant HDPs. Such discovery would enrich our comprehension of the function and evolution of the plant immune system, and provide us with novel molecular tools to develop innovative strategies to control crop diseases.
Additional Links: PMID-32973760
PubMed:
Citation:
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@article {pmid32973760,
year = {2020},
author = {Petre, B},
title = {Toward the Discovery of Host-Defense Peptides in Plants.},
journal = {Frontiers in immunology},
volume = {11},
number = {},
pages = {1825},
pmid = {32973760},
issn = {1664-3224},
abstract = {Defense peptides protect multicellular eukaryotes from infections. In biomedical sciences, a dominant conceptual framework refers to defense peptides as host-defense peptides (HDPs), which are bifunctional peptides with both direct antimicrobial and immunomodulatory activities. No HDP has been reported in plants so far, and the very concept of HDP has not been captured yet by the plant science community. Plant science thus lacks the conceptual framework that would coordinate research efforts aimed at discovering plant HDPs. In this perspective article, I used bibliometric and literature survey approaches to raise awareness about the HDP concept among plant scientists, and to encourage research efforts aimed at discovering plant HDPs. Such discovery would enrich our comprehension of the function and evolution of the plant immune system, and provide us with novel molecular tools to develop innovative strategies to control crop diseases.},
}
RevDate: 2020-09-28
Integrating genetic and nongenetic drivers of somatic evolution during carcinogenesis: The biplane model.
Evolutionary applications, 13(7):1651-1659.
The multistep transition from a normal to a malignant cellular phenotype is often termed "somatic evolution" caused by accumulating random mutations. Here, we propose an alternative model in which the initial genetic state of a cancer cell is the result of mutations that occurred throughout the lifetime of the host. However, these mutations are not carcinogenic because normal cells in multicellular organism cannot ordinarily evolve. That is, proliferation and death of normal cells are controlled by local tissue constraints typically governed by nongenomic information dynamics in the cell membrane. As a result, the cells of a multicellular organism have a fitness that is identical to the host, which is then the unit of natural selection. Somatic evolution of a cell can occur only when its fate becomes independent of host constraints. Now, survival, proliferation, and death of individual cells are dependent on Darwinian dynamics. This cellular transition from host-defined fitness to self-defined fitness may, consistent with the conventional view of carcinogenesis, result from mutations that render the cell insensitive to host controls. However, an identical state will result when surrounding tissue cannot exert control because of injury, inflammation, aging, or infection. Here, all surviving cells within the site of tissue damage default to self-defined fitness functions allowing them to evolve so that the mutations accumulated over the lifetime of the host now serve as the genetic heritage of an evolutionary unit of selection. Furthermore, tissue injury generates a new ecology cytokines and growth factors that might promote proliferation in cells with prior receptor mutations. This model integrates genetic and nongenetic dynamics into cancer development and is consistent with both clinical observations and prior experiments that divided carcinogenesis to initiation, promotion, and progression steps.
Additional Links: PMID-32952610
PubMed:
Citation:
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@article {pmid32952610,
year = {2020},
author = {Gatenby, RA and Avdieiev, S and Tsai, KY and Brown, JS},
title = {Integrating genetic and nongenetic drivers of somatic evolution during carcinogenesis: The biplane model.},
journal = {Evolutionary applications},
volume = {13},
number = {7},
pages = {1651-1659},
pmid = {32952610},
issn = {1752-4571},
support = {U54 CA143970/CA/NCI NIH HHS/United States ; },
abstract = {The multistep transition from a normal to a malignant cellular phenotype is often termed "somatic evolution" caused by accumulating random mutations. Here, we propose an alternative model in which the initial genetic state of a cancer cell is the result of mutations that occurred throughout the lifetime of the host. However, these mutations are not carcinogenic because normal cells in multicellular organism cannot ordinarily evolve. That is, proliferation and death of normal cells are controlled by local tissue constraints typically governed by nongenomic information dynamics in the cell membrane. As a result, the cells of a multicellular organism have a fitness that is identical to the host, which is then the unit of natural selection. Somatic evolution of a cell can occur only when its fate becomes independent of host constraints. Now, survival, proliferation, and death of individual cells are dependent on Darwinian dynamics. This cellular transition from host-defined fitness to self-defined fitness may, consistent with the conventional view of carcinogenesis, result from mutations that render the cell insensitive to host controls. However, an identical state will result when surrounding tissue cannot exert control because of injury, inflammation, aging, or infection. Here, all surviving cells within the site of tissue damage default to self-defined fitness functions allowing them to evolve so that the mutations accumulated over the lifetime of the host now serve as the genetic heritage of an evolutionary unit of selection. Furthermore, tissue injury generates a new ecology cytokines and growth factors that might promote proliferation in cells with prior receptor mutations. This model integrates genetic and nongenetic dynamics into cancer development and is consistent with both clinical observations and prior experiments that divided carcinogenesis to initiation, promotion, and progression steps.},
}
RevDate: 2020-11-13
Topological constraints in early multicellularity favor reproductive division of labor.
eLife, 9:.
Reproductive division of labor (e.g. germ-soma specialization) is a hallmark of the evolution of multicellularity, signifying the emergence of a new type of individual and facilitating the evolution of increased organismal complexity. A large body of work from evolutionary biology, economics, and ecology has shown that specialization is beneficial when further division of labor produces an accelerating increase in absolute productivity (i.e. productivity is a convex function of specialization). Here we show that reproductive specialization is qualitatively different from classical models of resource sharing, and can evolve even when the benefits of specialization are saturating (i.e. productivity is a concave function of specialization). Through analytical theory and evolutionary individual-based simulations, we demonstrate that reproductive specialization is strongly favored in sparse networks of cellular interactions that reflect the morphology of early, simple multicellular organisms, highlighting the importance of restricted social interactions in the evolution of reproductive specialization.
Additional Links: PMID-32940598
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Citation:
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@article {pmid32940598,
year = {2020},
author = {Yanni, D and Jacobeen, S and Márquez-Zacarías, P and Weitz, JS and Ratcliff, WC and Yunker, PJ},
title = {Topological constraints in early multicellularity favor reproductive division of labor.},
journal = {eLife},
volume = {9},
number = {},
pages = {},
pmid = {32940598},
issn = {2050-084X},
support = {IOS-1656549//National Science Foundation/International ; GM138030/NH/NIH HHS/United States ; BMAT-2003721//National Science Foundation/International ; },
abstract = {Reproductive division of labor (e.g. germ-soma specialization) is a hallmark of the evolution of multicellularity, signifying the emergence of a new type of individual and facilitating the evolution of increased organismal complexity. A large body of work from evolutionary biology, economics, and ecology has shown that specialization is beneficial when further division of labor produces an accelerating increase in absolute productivity (i.e. productivity is a convex function of specialization). Here we show that reproductive specialization is qualitatively different from classical models of resource sharing, and can evolve even when the benefits of specialization are saturating (i.e. productivity is a concave function of specialization). Through analytical theory and evolutionary individual-based simulations, we demonstrate that reproductive specialization is strongly favored in sparse networks of cellular interactions that reflect the morphology of early, simple multicellular organisms, highlighting the importance of restricted social interactions in the evolution of reproductive specialization.},
}
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ESP Quick Facts
ESP Origins
In the early 1990's, Robert Robbins was a faculty member at Johns Hopkins, where he directed the informatics core of GDB — the human gene-mapping database of the international human genome project. To share papers with colleagues around the world, he set up a small paper-sharing section on his personal web page. This small project evolved into The Electronic Scholarly Publishing Project.
ESP Support
In 1995, Robbins became the VP/IT of the Fred Hutchinson Cancer Research Center in Seattle, WA. Soon after arriving in Seattle, Robbins secured funding, through the ELSI component of the US Human Genome Project, to create the original ESP.ORG web site, with the formal goal of providing free, world-wide access to the literature of classical genetics.
ESP Rationale
Although the methods of molecular biology can seem almost magical to the uninitiated, the original techniques of classical genetics are readily appreciated by one and all: cross individuals that differ in some inherited trait, collect all of the progeny, score their attributes, and propose mechanisms to explain the patterns of inheritance observed.
ESP Goal
In reading the early works of classical genetics, one is drawn, almost inexorably, into ever more complex models, until molecular explanations begin to seem both necessary and natural. At that point, the tools for understanding genome research are at hand. Assisting readers reach this point was the original goal of The Electronic Scholarly Publishing Project.
ESP Usage
Usage of the site grew rapidly and has remained high. Faculty began to use the site for their assigned readings. Other on-line publishers, ranging from The New York Times to Nature referenced ESP materials in their own publications. Nobel laureates (e.g., Joshua Lederberg) regularly used the site and even wrote to suggest changes and improvements.
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When the site began, no journals were making their early content available in digital format. As a result, ESP was obliged to digitize classic literature before it could be made available. For many important papers — such as Mendel's original paper or the first genetic map — ESP had to produce entirely new typeset versions of the works, if they were to be available in a high-quality format.
ESP Help
Early support from the DOE component of the Human Genome Project was critically important for getting the ESP project on a firm foundation. Since that funding ended (nearly 20 years ago), the project has been operated as a purely volunteer effort. Anyone wishing to assist in these efforts should send an email to Robbins.
ESP Plans
With the development of methods for adding typeset side notes to PDF files, the ESP project now plans to add annotated versions of some classical papers to its holdings. We also plan to add new reference and pedagogical material. We have already started providing regularly updated, comprehensive bibliographies to the ESP.ORG site.
ESP Picks from Around the Web (updated 07 JUL 2018 )
Old Science
Weird Science
Treating Disease with Fecal Transplantation
Fossils of miniature humans (hobbits) discovered in Indonesia
Paleontology
Dinosaur tail, complete with feathers, found preserved in amber.
Astronomy
Mysterious fast radio burst (FRB) detected in the distant universe.
Big Data & Informatics
Big Data: Buzzword or Big Deal?
Hacking the genome: Identifying anonymized human subjects using publicly available data.