The causes of epistasis
Since Bateson's discovery that genes can suppress the phenotypic effects of other genes, gene interactions—called epistasis—have been the topic of a vast research effort. Systems and developmental biologists study epistasis to understand the genotype–phenotype map, whereas evolutionary biologis...
| Autores: | , , , |
|---|---|
| Tipo de recurso: | artículo |
| Fecha de publicación: | 2011 |
| País: | España |
| Institución: | Consejo Superior de Investigaciones Científicas (CSIC) |
| Repositorio: | DIGITAL.CSIC. Repositorio Institucional del CSIC |
| OAI Identifier: | oai:digital.csic.es:10261/48711 |
| Acceso en línea: | http://hdl.handle.net/10261/48711 |
| Access Level: | acceso abierto |
| Palabra clave: | Robustness Evolvability Epistasis Pleiotropy |
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The causes of epistasisDe Visser, J.Cooper, Tim F.Elena, Santiago F.Arjan, G. M.RobustnessEvolvabilityEpistasisPleiotropySince Bateson's discovery that genes can suppress the phenotypic effects of other genes, gene interactions—called epistasis—have been the topic of a vast research effort. Systems and developmental biologists study epistasis to understand the genotype–phenotype map, whereas evolutionary biologists recognize the fundamental importance of epistasis for evolution. Depending on its form, epistasis may lead to divergence and speciation, provide evolutionary benefits to sex and affect the robustness and evolvability of organisms. That epistasis can itself be shaped by evolution has only recently been realized. Here, we review the empirical pattern of epistasis, and some of the factors that may affect the form and extent of epistasis. Based on their divergent consequences, we distinguish between interactions with or without mean effect, and those affecting the magnitude of fitness effects or their sign. Empirical work has begun to quantify epistasis in multiple dimensions in the context of metabolic and fitness landscape models. We discuss possible proximate causes (such as protein function and metabolic networks) and ultimate factors (including mutation, recombination, and the importance of natural selection and genetic drift). We conclude that, in general, pleiotropy is an important prerequisite for epistasis, and that epistasis may evolve as an adaptive or intrinsic consequence of changes in genetic robustness and evolvability.We thank Fons Debets, Ryszard Korona, Alexey Kondrashov, Joachim Krug, Sijmen Schoustra and an anonymous reviewer for constructive comments, and funds from the European Union Seventh Framework Programme (FP7/2007-2013) under grant agreement 225167 (e-FLUX), a visitor grant from Research School Production Ecology and Resource Conservation for S.F.E., and NSF grant DEB-0844355 for T.F.C.Peer reviewedRoyal Society (Great Britain)201220122011info:eu-repo/semantics/articlehttp://purl.org/coar/resource_type/c_6501http://hdl.handle.net/10261/48711reponame:DIGITAL.CSIC. Repositorio Institucional del CSICinstname:Consejo Superior de Investigaciones Científicas (CSIC)Inglésinfo:eu-repo/semantics/openAccessoai:digital.csic.es:10261/487112026-05-22T06:33:51Z |
| dc.title.none.fl_str_mv |
The causes of epistasis |
| title |
The causes of epistasis |
| spellingShingle |
The causes of epistasis De Visser, J. Robustness Evolvability Epistasis Pleiotropy |
| title_short |
The causes of epistasis |
| title_full |
The causes of epistasis |
| title_fullStr |
The causes of epistasis |
| title_full_unstemmed |
The causes of epistasis |
| title_sort |
The causes of epistasis |
| dc.creator.none.fl_str_mv |
De Visser, J. Cooper, Tim F. Elena, Santiago F. Arjan, G. M. |
| author |
De Visser, J. |
| author_facet |
De Visser, J. Cooper, Tim F. Elena, Santiago F. Arjan, G. M. |
| author_role |
author |
| author2 |
Cooper, Tim F. Elena, Santiago F. Arjan, G. M. |
| author2_role |
author author author |
| dc.subject.none.fl_str_mv |
Robustness Evolvability Epistasis Pleiotropy |
| topic |
Robustness Evolvability Epistasis Pleiotropy |
| description |
Since Bateson's discovery that genes can suppress the phenotypic effects of other genes, gene interactions—called epistasis—have been the topic of a vast research effort. Systems and developmental biologists study epistasis to understand the genotype–phenotype map, whereas evolutionary biologists recognize the fundamental importance of epistasis for evolution. Depending on its form, epistasis may lead to divergence and speciation, provide evolutionary benefits to sex and affect the robustness and evolvability of organisms. That epistasis can itself be shaped by evolution has only recently been realized. Here, we review the empirical pattern of epistasis, and some of the factors that may affect the form and extent of epistasis. Based on their divergent consequences, we distinguish between interactions with or without mean effect, and those affecting the magnitude of fitness effects or their sign. Empirical work has begun to quantify epistasis in multiple dimensions in the context of metabolic and fitness landscape models. We discuss possible proximate causes (such as protein function and metabolic networks) and ultimate factors (including mutation, recombination, and the importance of natural selection and genetic drift). We conclude that, in general, pleiotropy is an important prerequisite for epistasis, and that epistasis may evolve as an adaptive or intrinsic consequence of changes in genetic robustness and evolvability. |
| publishDate |
2011 |
| dc.date.none.fl_str_mv |
2011 2012 2012 |
| dc.type.none.fl_str_mv |
info:eu-repo/semantics/article http://purl.org/coar/resource_type/c_6501 |
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article |
| dc.identifier.none.fl_str_mv |
http://hdl.handle.net/10261/48711 |
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http://hdl.handle.net/10261/48711 |
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Inglés |
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Inglés |
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info:eu-repo/semantics/openAccess |
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openAccess |
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Royal Society (Great Britain) |
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Royal Society (Great Britain) |
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reponame:DIGITAL.CSIC. Repositorio Institucional del CSIC instname:Consejo Superior de Investigaciones Científicas (CSIC) |
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Consejo Superior de Investigaciones Científicas (CSIC) |
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DIGITAL.CSIC. Repositorio Institucional del CSIC |
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DIGITAL.CSIC. Repositorio Institucional del CSIC |
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15,811543 |