Evidence for a genetic basis of aging in two wild vertebrate populations

Evidence for a genetic basis of aging in two wild vertebrate populations. Wilson, A., J., Nussey, D., H., Pemberton, J., M., Pilkington, J., G., Morris, A., Pelletier, F., Clutton-Brock, T., H., & Kruuk, L., E. Current Biology, 17(24):2136-2142, 12, 2007.

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Aging, or senescence, defined as a decline in physiological function with age, has long been a focus of research interest for evolutionary biologists. How has natural selection failed to remove genetic effects responsible for such reduced fitness among older individuals? Current evolutionary theory explains this phenomenon by showing that, as a result of the risk of death from environmental causes that individuals experience, the force of selection inevitably weakens with age [1-3]. This in turn means that genetic mutations having detrimental effects that are only felt late in life might persist in a population. Although widely accepted, this theory rests on the assumption that there is genetic variation for aging in natural systems [4, 5], or (equivalently), that genotype-by-age interactions (GxA) occur for fitness. To date, empirical support for this assumption has come almost entirely from laboratory studies on invertebrate systems, most notably Drosophila and C. elegans [6-10], whereas tests of genetic variation for aging are largely lacking from natural populations [5]. By using data from two wild mammal populations, we perform quantitative genetic analyses of fitness and provide the first evidence for a genetic basis of senescence to come from a study in the natural environment. We find evidence that genetic differences among individuals cause variation in their rates of aging and that additive genetic variance for fitness increases with age, as predicted by the evolutionary theory of senescence. © 2007 Elsevier Ltd. All rights reserved.

@article{
 title = {Evidence for a genetic basis of aging in two wild vertebrate populations},
 type = {article},
 year = {2007},
 keywords = {EVO_ECOL},
 pages = {2136-2142},
 volume = {17},
 websites = {https://linkinghub.elsevier.com/retrieve/pii/S0960982207022828},
 month = {12},
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 abstract = {Aging, or senescence, defined as a decline in physiological function with age, has long been a focus of research interest for evolutionary biologists. How has natural selection failed to remove genetic effects responsible for such reduced fitness among older individuals? Current evolutionary theory explains this phenomenon by showing that, as a result of the risk of death from environmental causes that individuals experience, the force of selection inevitably weakens with age [1-3]. This in turn means that genetic mutations having detrimental effects that are only felt late in life might persist in a population. Although widely accepted, this theory rests on the assumption that there is genetic variation for aging in natural systems [4, 5], or (equivalently), that genotype-by-age interactions (GxA) occur for fitness. To date, empirical support for this assumption has come almost entirely from laboratory studies on invertebrate systems, most notably Drosophila and C. elegans [6-10], whereas tests of genetic variation for aging are largely lacking from natural populations [5]. By using data from two wild mammal populations, we perform quantitative genetic analyses of fitness and provide the first evidence for a genetic basis of senescence to come from a study in the natural environment. We find evidence that genetic differences among individuals cause variation in their rates of aging and that additive genetic variance for fitness increases with age, as predicted by the evolutionary theory of senescence. © 2007 Elsevier Ltd. All rights reserved.},
 bibtype = {article},
 author = {Wilson, Alastair J. and Nussey, Daniel H. and Pemberton, Josephine M. and Pilkington, Jill G. and Morris, Alison and Pelletier, Fanie and Clutton-Brock, Timothy H. and Kruuk, Loeske E.B.},
 doi = {10.1016/j.cub.2007.11.043},
 journal = {Current Biology},
 number = {24}
}

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