Sanjuán Rafael, Elena Santiago F
Instituto de Biología Molecular y Celular de Plantas, Consejo Superior de Investigaciones Científicas-UPV, 46022 València, Spain.
Proc Natl Acad Sci U S A. 2006 Sep 26;103(39):14402-5. doi: 10.1073/pnas.0604543103. Epub 2006 Sep 18.
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.
在进化生物学中，基因组规模上是否存在系统性基因相互作用（上位性）仍是一个具有挑战性的课题。上位性理应会对复杂性状的变异做出重大贡献，并影响诸如性别、二倍体、显性或基因组被有害突变污染等遗传系统的进化。我们从广泛不同的生物体收集了数据，并在一个共同的每代尺度上对上位性进行了量化。更简单的基因组，如RNA病毒的基因组，表现出拮抗上位性（突变共同产生的影响小于预期）；细菌微生物显然没有偏离独立效应，而在多细胞真核生物中，则出现了向协同上位性的转变（突变共同产生的影响大于预期）。我们提出，拮抗上位性可能是具有很少非多效性生物学功能的紧凑基因组的一个特性，而在复杂基因组中，协同性可能源自突变稳健性。
