Department of Genetics, University of Georgia, Athens, GA, USA.
J Evol Biol. 2009 Dec;22(12):2409-19. doi: 10.1111/j.1420-9101.2009.01849.x. Epub 2009 Oct 12.
One of the two main hypotheses to account for ageing is antagonistic pleiotropy (AP). This model requires alleles that increase vital rates (reproduction or survival) at early age at the expense of vital rates at late age. An important focus of evolutionary studies has been to assess the relative abundance of AP-type aging alleles that arise through mutation. Here, we develop theory that predicts that senescence per se reduces the probability that these alleles arise by mutation. A direct result is that these mutations should arise with extremely low frequencies in already senescing populations. This has profound implications for the evolution of life histories because it implies that the adaptive evolution of aging via AP will experience negative feedback. This theory also clarifies the previously inexplicable epistatic patterns of genetic covariance across age-specific vital rates that are observed in mutation accumulation experiments. We show that this epistasis is an emergent property of aging.
两种主要的衰老假说之一是拮抗性多效性（AP）。该模型需要等位基因以牺牲晚年的生命率（繁殖或生存）为代价来提高早期的生命率。进化研究的一个重要焦点一直是评估通过突变产生的 AP 型衰老等位基因的相对丰度。在这里，我们提出了一个理论，该理论预测衰老本身会降低这些等位基因通过突变产生的可能性。一个直接的结果是，这些突变在已经衰老的种群中应该以极低的频率出现。这对生命史的进化有深远的影响，因为这意味着通过 AP 进行衰老的适应性进化将受到负反馈。该理论还澄清了在突变积累实验中观察到的年龄特定生命率的遗传协方差的先前无法解释的上位模式。我们表明，这种上位性是衰老的一种突现特性。
