Ageing Research Group, Department of Animal Ecology, Evolutionary Biology Centre, Uppsala University, , Uppsala, Norbyvägen 18D 75236, Sweden.
Biol Lett. 2013 Oct 2;9(5):20130217. doi: 10.1098/rsbl.2013.0217. Print 2013 Oct 23.
While ageing is commonly associated with exponential increase in mortality with age, mortality rates paradoxically decelerate late in life resulting in distinct mortality plateaus. Late-life mortality plateaus have been discovered in a broad variety of taxa, including humans, but their origin is hotly debated. One hypothesis argues that deceleration occurs because the individual probability of death stops increasing at very old ages, predicting the evolution of earlier onset of mortality plateaus under increased rate of extrinsic mortality. By contrast, heterogeneity theory suggests that mortality deceleration arises from individual differences in intrinsic lifelong robustness and predicts that variation in robustness between populations will result in differences in mortality deceleration. We used experimental evolution to directly test these predictions by independently manipulating extrinsic mortality rate (high or low) and mortality source (random death or condition-dependent) to create replicate populations of nematodes, Caenorhabditis remanei that differ in the strength of selection in late-life and in the level of lifelong robustness. Late-life mortality deceleration evolved in response to differences in mortality source when mortality rate was held constant, while there was no consistent response to differences in mortality rate. These results provide direct experimental support for the heterogeneity theory of late-life mortality deceleration.
虽然衰老通常与年龄相关的死亡率呈指数增长有关，但死亡率在生命后期却出人意料地减缓，导致明显的死亡率稳定期。在包括人类在内的广泛生物类群中都发现了老年死亡率稳定期，但它们的起源仍存在争议。一种假设认为，减速是因为个体死亡的概率在非常高龄时停止增加，这预测了在外部死亡率增加的情况下，死亡率稳定期会更早出现。相比之下，异质性理论认为，死亡率减速是由于个体内在终身稳健性的差异造成的，并预测种群之间稳健性的差异将导致死亡率减速的差异。我们通过独立操纵外在死亡率（高或低）和死亡源（随机死亡或条件相关），创造了具有不同老年期选择强度和终身稳健性水平的实验演化复制线虫种群 Caenorhabditis remanei，直接检验了这些预测。当死亡率保持不变时，死亡率源的差异导致了老年期死亡率的减速，而死亡率的差异则没有一致的响应。这些结果为老年期死亡率减速的异质性理论提供了直接的实验支持。
