The worm that lived: Evolution of rapid aging under high extrinsic mortality revisited.
The worm that lived: Evolution of rapid aging under high extrinsic mortality revisited.
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DOI：
10.4161/worm.23704
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发表时间：
2013-07-01
期刊：
影响因子：
--
通讯作者：
Maklakov AA
中科院分区：
文献类型：
--
作者：
Chen HY;Maklakov AA
生物衰老是因为“选择阴影”--自然选择的力量随着年龄的增长而减弱。这一理论的一个看似简单的推论是梅达沃-威廉姆斯预测，该预测认为外在（非衰老）死亡率的增加将导致加速衰老和寿命缩短的演变。尽管这一预测对现代人关于衰老的最终原因的思考至关重要，但它忽略了一个事实，即死亡往往是一个取决于个人状况的非随机过程。条件依赖性死亡率的增加不可避免地导致对死亡因子的抗性的选择增加。假设对各种压力的抵抗力通常与寿命的延长有关，那么进化的结果就不再确定了。我们最近通过实验证明了这一点，表明在高的外在死亡率下，瑞氏小杆线虫种群的寿命会缩短，但只有在死亡率被随机应用时。相反，当外在死亡率是由热休克，人口经历了相同的死亡率增加进化更长的寿命，尽管增加了“选择阴影”。有趣的是，抗压力和长寿的蠕虫也更能繁殖。我们讨论了这些结果，在最近的理论发展，如条件-环境相互作用和衰老的机能亢进理论。
Organisms age because of the “selection shadow”—the decline of the force of natural selection with age. Seemingly straightforward corollary of this theory is the Medawar-Williams prediction, which maintains that increased extrinsic (non-aging) mortality will result in the evolution of accelerated aging and decreased longevity. Despite its centrality to modern thinking about the ultimate causes of aging, this prediction ignores the fact that mortality is often a non-random process depending on individual condition. Increased condition-dependent mortality inescapably results in increased selection for resistance against the agent of mortality. Provided that resistance to various stressors is commonly associated with increased longevity, the evolutionary outcome is no longer certain. We recently documented this experimentally by showing that populations of Caenorhabditis remanei evolved to live shorter under high extrinsic mortality, but only when mortality was applied haphazardly. On the contrary, when extrinsic mortality was caused by heat-shock, populations experiencing the same rate of increased mortality evolved greater longevities, notwithstanding increased “selection shadow.” Intriguingly, stress-resistant and long-lived worms were also more fecund. We discuss these results in the light of recent theoretical developments, such as condition-environment interactions and hyperfunction theory of aging.