Rose Michael R, Drapeau Mark D, Yazdi Puya G, Shah Kandarp H, Moise Diana B, Thakar Rena R, Rauser Casandra L, Mueller Laurence D
Department of Ecology and Evolutionary Biology, University of California, Irvine 92697, USA.
Evolution. 2002 Oct;56(10):1982-91. doi: 10.1111/j.0014-3820.2002.tb00124.x.
Aging appears to cease at late ages, when mortality rates roughly plateau in large-scale demographic studies. This anomalous plateau in late-life mortality has been explained theoretically in two ways: (1) as a strictly demographic result of heterogeneity in life-long robustness between individuals within cohorts, and (2) as an evolutionary result of the plateau in the force of natural selection after the end of reproduction. Here we test the latter theory using cohorts of Drosophila melanogaster cultured with different ages of reproduction for many generations. We show in two independent comparisons that populations that evolve with early truncation of reproduction exhibit earlier onset of mortality-rate plateaus, in conformity with evolutionary theory. In addition, we test two population genetic mechanisms that may be involved in the evolution of late-life mortality: mutation accumulation and antagonistic pleiotropy. We test mutation accumulation by crossing genetically divergent, yet demographically identical, populations, testing for hybrid vigor between the hybrid and nonhybrid parental populations. We found no difference between the hybrid and nonhybrid populations in late-life mortality rates, a result that does not support mutation accumulation as a genetic mechanism for late-life mortality, assuming mutations act recessively. Finally, we test antagonistic pleiotropy by returning replicate populations to a much earlier age of last reproduction for a short evolutionary time, testing for a rapid indirect response of late-life mortality rates. The positive results from this test support antagonistic pleiotropy as a genetic mechanism for the evolution of late-life mortality. Together these experiments comprise the first corroborations of the evolutionary theory of late-life mortality.
在大规模人口统计学研究中,死亡率大致趋于平稳时,衰老似乎在高龄阶段停止。关于晚年死亡率这种异常的平稳状态,理论上有两种解释:(1)作为同一队列中个体终身强健性存在异质性的严格人口统计学结果;(2)作为繁殖结束后自然选择力趋于平稳的进化结果。在此,我们使用多代繁殖年龄不同的黑腹果蝇群体来检验后一种理论。我们在两项独立比较中表明,随着繁殖提前截断而进化的群体,其死亡率平稳期出现得更早,这与进化理论相符。此外,我们检验了可能参与晚年死亡率进化的两种群体遗传机制:突变积累和拮抗多效性。我们通过让遗传上有差异但人口统计学特征相同的群体杂交来检验突变积累,检测杂交群体与非杂交亲本群体之间的杂种优势。我们发现杂交群体和非杂交群体在晚年死亡率上没有差异,这一结果不支持突变积累作为晚年死亡率的遗传机制,前提是突变起隐性作用。最后,我们通过让重复群体在较短的进化时间内回到更早的最后繁殖年龄来检验拮抗多效性,检测晚年死亡率的快速间接反应。该检验的阳性结果支持拮抗多效性作为晚年死亡率进化的遗传机制。这些实验共同构成了对晚年死亡率进化理论的首次验证。