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. 2009 Jun 22;276(1665):2271-8.
doi: 10.1098/rspb.2009.0183. Epub 2009 Mar 18.

What Can Genetic Variation Tell Us About the Evolution of Senescence?

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Free PMC article

What Can Genetic Variation Tell Us About the Evolution of Senescence?

Jacob A Moorad et al. Proc Biol Sci. .
Free PMC article

Abstract

Quantitative genetic approaches have been developed that allow researchers to determine which of two mechanisms, mutation accumulation (MA) or antagonistic pleiotropy (AP), best explain observed variation in patterns of senescence using classical quantitative genetic techniques. These include the creation of mutation accumulation lines, artificial selection experiments and the partitioning of genetic variances across age classes. This last strategy has received the lion's share of empirical attention. Models predict that inbreeding depression (ID), dominance variance and the variance among inbred line means will all increase with age under MA but not under those forms of AP that generate marginal overdominance. Here, we show that these measures are not, in fact, diagnostic of MA versus AP. In particular, the assumptions about the value of genetic parameters in existing AP models may be rather narrow, and often violated in reality. We argue that whenever ageing-related AP loci contribute to segregating genetic variation, polymorphism at these loci will be enhanced by genetic effects that will also cause ID and dominance variance to increase with age, effects also expected under the MA model of senescence. We suggest that the tests that seek to identify the relative contributions of AP and MA to the evolution of ageing by partitioning genetic variance components are likely to be too conservative to be of general value.

Figures

Figure 1
Figure 1
AP models for marginal overdominance. (a) Age-specific genetic effects on (i) phenotype and (ii) fitness under the Charlesworth–Hughes (CH) model of AP. (b) Age-specific genetic effects on (i) phenotype and (ii) fitness under a more stable model of AP. The thick solid lines indicate the genetic value of homozygote 11, the thin solid lines are the values of the alternative homozygote 22, and the intermediately solid lines indicate the value of the heterozygotes. The dashed lines are average of homozygote values. CH assume equal additive effects on phenotypes across ages (indicated by the vertical lengths of brackets on a(i)). They also assume equal dominance effects (double-headed arrows). This requires that ID and dominance variance will not change with age (equation (2.1) in the text). (a(ii)) The additive and dominance effects on the fitness scale decline with age because early-age traits (x) are more relevant to fitness than late-age traits (y). All else being equal, (b(ii)) the stability of these polymorphisms increases with increased symmetry of homozygote effects on the scale of fitness. (b(i)) With ageing, maximum stability is reached when additive and dominance effects on the phenotypic scale are greatest at late age. This causes additive genetic variance, dominance variance and ID to increase with age.
Figure 2
Figure 2
AP conditions that require increased dominance with age. The shaded region indicates that dominance must increase with age in order to generate variation by balancing selection. The horizontal axis is the amount of dominance at early age divided by the additive effect (e.g. 0 corresponds to additivity and 1 to complete dominance). The vertical axis is the fitness relevance of the phenotype at late age divided by that at early age. This assumes that additive effects are constant across age. Large differences in ages (low β) will require dominance to increase unless early-age dominance is very high.

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