Wagner A
Department of Biology, University of New Mexico, and The Santa Fe Institute, Albuquerque, NM, USA.
Nat Genet. 2000 Apr;24(4):355-61. doi: 10.1038/74174.
There are two principal mechanisms that are responsible for the ability of an organism's physiological and developmental processes to compensate for mutations. In the first, genes have overlapping functions, and loss-of-function mutations in one gene will have little phenotypic effect if there are one or more additional genes with similar functions. The second mechanism has its origin in interactions between genes with unrelated functions, and has been documented in metabolic and regulatory gene networks. Here I analyse, on a genome-wide scale, which of these mechanisms of robustness against mutations is more prevalent. I used functional genomics data from the yeast Saccharomyces cerevisiae to test hypotheses related to the following: if gene duplications are mostly responsible for robustness, then a correlation is expected between the similarity of two duplicated genes and the effect of mutations in one of these genes. My results demonstrate that interactions among unrelated genes are the major cause of robustness against mutations. This type of robustness is probably an evolved response of genetic networks to stabilizing selection.
生物体的生理和发育过程能够补偿突变，这主要有两种机制。第一种机制是，基因具有重叠功能，若存在一个或多个具有相似功能的其他基因，那么其中一个基因的功能丧失突变对表型的影响就很小。第二种机制源于功能不相关基因之间的相互作用，在代谢和调控基因网络中已有记载。在此，我在全基因组范围内分析这两种抗突变稳健性机制中哪种更为普遍。我使用来自酿酒酵母的功能基因组学数据来检验与以下内容相关的假设：如果基因复制主要负责稳健性，那么预期两个复制基因的相似性与其中一个基因中的突变效应之间存在相关性。我的结果表明，不相关基因之间的相互作用是抗突变稳健性的主要原因。这种稳健性类型可能是遗传网络对稳定选择的一种进化反应。
