Kin competition, natal dispersal and the moulding of senescence by natural selection
Kin competition, natal dispersal and the moulding of senescence by natural selection
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亲缘竞争、出生扩散和自然选择导致的衰老塑造
DOI：
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发表时间：
2010
期刊：
影响因子：
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通讯作者：
D. Promislow
中科院分区：
文献类型：
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作者：
O. Ronce;D. Promislow
大多数衰老进化的理论模型都假设了一个非常大的、混合良好的种群。在这里，我们通过推导选择力量的指标，研究有限的分散和亲属竞争可能如何影响衰老的进化，类似于汉密尔顿(Hamilton，1966 J.Theor)。比奥尔。12、12-45)。我们的分析模型描述了在一个零星的种群中，成虫是属地的，少部分幼虫分散在不同的领地，对生存和繁殖力的选择强度如何随着年龄的变化而变化。然后，亲子竞争和同胞竞争都会影响特定年龄的生活史特征的选择。亲缘竞争降低了生存选择的强度。在某些年龄段，增加死亡率的突变甚至可以通过选择来支持，但只有在生育能力随着年龄迅速恶化的情况下才会如此。然而，由于有限的扩散而产生的种群结构选择了一生中更广泛的生殖分布，潜在地减缓了生殖衰老。有限的扩散对生育和死亡的年龄时间表产生的对抗作用，让人怀疑条件的普遍性，这些条件允许在没有其他直接多效性影响的情况下，进化出增加死亡率的“自杀基因”。更广泛地说，我们的模型说明了有限的分散和社会互动如何间接地产生拮抗多效性模式，影响不同年龄的生命频率。
Most theoretical models for the evolution of senescence have assumed a very large, well mixed population. Here, we investigate how limited dispersal and kin competition might influence the evolution of ageing by deriving indicators of the force of selection, similar to Hamilton (Hamilton 1966 J. Theor. Biol. 12, 12–45). Our analytical model describes how the strength of selection on survival and fecundity changes with age in a patchy population, where adults are territorial and a fraction of juveniles disperse between territories. Both parent–offspring competition and sib competition then affect selection on age-specific life-history traits. Kin competition reduces the strength of selection on survival. Mutations increasing mortality in some age classes can even be favoured by selection, but only when fecundity deteriorates rapidly with age. Population structure arising from limited dispersal however selects for a broader distribution of reproduction over the lifetime, potentially slowing down reproductive senescence. The antagonistic effects of limited dispersal on age schedules of fecundity and mortality cast doubts on the generality of conditions allowing the evolution of ‘suicide genes’ that increase mortality rates without other direct pleiotropic effects. More generally, our model illustrates how limited dispersal and social interactions can indirectly produce patterns of antagonistic pleiotropy affecting vital rates at different ages.