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Título: | Epistasis correlates to genomic complexity |
Autor: | Sanjuán, Rafael CSIC ORCID; Elena, Santiago F. CSIC ORCID | Palabras clave: | Mutation Robustness Antagonisms Evolution Synergism |
Fecha de publicación: | 18-sep-2006 | Editor: | National Academy of Sciences (U.S.) | Citación: | Proc. Natl. Acad. Sci. USA 103(39): 14402-14405 (2006) | Resumen: | Whether systematic genetic interactions (epistasis) occur at the genomic scale remains a challenging topic in evolutionary biology. Epistasis should make a significant contribution to variation in complex traits and influence the evolution of genetic systems as sex, diploidy, dominance, or the contamination of genomes with deleterious mutations. We have collected data from widely different organisms and quantified epistasis in a common, per-generation scale. Simpler genomes, such as those of RNA viruses, display antagonistic epistasis (mutations have smaller effects together than expected); bacterial microorganisms do not apparently deviate from independent effects, whereas in multicellular eukaryotes, a transition toward synergistic epistasis occurs (mutations have larger effects together than expected). We propose that antagonistic epistasis might be a property of compact genomes with few nonpleiotropic biological functions, whereas in complex genomes, synergism might emerge from mutational robustness. | Descripción: | 4 pages, 2 figures.-- Additional information (Suppl. Table S2: Synopsis of the studies seeking for epistasis between deleterious mutations, and Suppl. text: Possible factors that could have led to an artefactual correlation between epistasis and genome complexity) available at: http://www.pnas.org/content/103/39/14402/suppl/DC1 | Versión del editor: | http://dx.doi.org/10.1073/pnas.0604543103 | URI: | http://hdl.handle.net/10261/9414 | DOI: | 10.1073/pnas.0604543103 | ISSN: | 0027-8424 |
Aparece en las colecciones: | (IBMCP) Artículos |
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