The degree to which changes in lifespan are coupled to changes in senescence in different physiological systems and phenotypic traits is a central question in biogerontology. It is underpinned by deeper biological questions about whether or not senescence is a synchronised process, or whether levels of synchrony depend on species or environmental context. Understanding how natural selection shapes patterns of synchrony in senescence across physiological systems and phenotypic traits demands the longitudinal study of many phenotypes under natural conditions. Here, we examine the patterns of age-related variation in late adulthood in a wild population of Soay sheep (Ovis aries) that have been the subject of individual-based monitoring for thirty years. We examined twenty different phenotypic traits in both males and females, encompassing vital rates (survival and fecundity), maternal reproductive performance (offspring birth weight, birth date and survival), male rutting behaviour, home range measures, parasite burdens, and body mass. We initially quantified age-related variation in each trait having controlled for annual variation in the environment, among-individual variation and selective disappearance effects. We then standardised our age-specific trait means and tested whether age trajectories could be meaningfully grouped according to sex or the type of trait. Whilst most traits showed age-related declines in later life, we found striking levels of asynchrony both within and between the sexes. Of particular note, female fecundity and reproductive performance declined with age, but male annual reproductive success did not. We also discovered that whilst home range size and quality decline with age in females, home range size increases with age in males. Our findings highlight the complexity of phenotypic ageing under natural conditions and, along with emerging data from other wild populations and laboratory models, suggest that the long-standing hypothesis within evolutionary biology that fitness-related traits should senesce in a synchronous manner is seriously flawed.
When relatives mate, their inbred offspring often suffer a reduction in fitness-related traits known as "inbreeding depression." There is mounting evidence that inbreeding depression can be exacerbated by environmental stresses such as starvation, predation, parasitism, and competition. Parental care may play an important role as a buffer against inbreeding depression in the offspring by alleviating these environmental stresses. Here, we examine the effect of parental care on the fitness costs of inbreeding in the burying beetle Nicrophorus vespilloides, an insect with facultative parental care. We used a 2 × 2 factorial design with the following factors: (i) the presence or absence of a caring female parent during larval development and (ii) inbred or outbred offspring. We examined the joint influence of maternal care and inbreeding status on fitness-related offspring traits to test the hypothesis that maternal care improves the performance of inbred offspring more than that of outbred offspring. Indeed, the female's presence led to a higher increase in larval survival in inbred than in outbred broods. Receiving care at the larval stage also increased the lifespan of inbred but not outbred adults, suggesting that the beneficial buffering effects of maternal care can persist long after the offspring have become independent. Our results show that parental care has the potential to moderate the severity of inbreeding depression, which in turn may favor inbreeding tolerance and influence the evolution of mating systems and other inbreedingavoidance mechanisms.parental care | environmental stress | fitness | inbreeding depression | inbreeding tolerance
Increased maternal age at reproduction is often associated with decreased offspring performance in numerous species of plants and animals (including humans). Current evolutionary theory considers such maternal effect senescence as part of a unified process of reproductive senescence, which is under identical age-specific selective pressures to fertility. We offer a novel theoretical perspective by combining William Hamilton's evolutionary model for aging with a quantitative genetic model of indirect genetic effects. We demonstrate that fertility and maternal effect senescence are likely to experience different patterns of age-specific selection and thus can evolve to take divergent forms. Applied to neonatal survival, we find that selection for maternal effects is the product of age-specific fertility and Hamilton's age-specific force of selection for fertility. Population genetic models show that senescence for these maternal effects can evolve in the absence of reproductive or actuarial senescence; this implies that maternal effect aging is a fundamentally distinct demographic manifestation of the evolution of aging. However, brief periods of increasingly beneficial maternal effects can evolve when fertility increases with age faster than cumulative survival declines. This is most likely to occur early in life. Our integration of theory provides a general framework with which to model, measure, and compare the evolutionary determinants of the social manifestations of aging. Extension of our maternal effects model to other ecological and social contexts could provide important insights into the drivers of the astonishing diversity of lifespans and aging patterns observed among species.S enescence is the age-related deterioration of organismal function and fitness. Evolutionary theory explains its pervasiveness as the result of age-related declines in the strength of natural selection to preserve survival and reproduction (1). Genes deleterious to survival or fertility in late life can persist or even come to fixation as a result of this weakening of selection in old age (2-4). To date, most theoretical and empirical research into the evolution of senescence has focused on age-specific survival and fertility (vital rates), as these rates are most proximate to fitness. Both age-related declines in survival (actuarial senescence) and fertility (reproductive senescence) can evolve independently from initially nonsenescent life histories (1).These vital rates are a product of complex interactions among different physiological systems, phenotypic traits, and their environment. One important source of environmental contributions involves social interactions. The influence of other individuals in the environment on a particular phenotype can itself be heritable, and the importance of these so-called "indirect genetic effects" (IGEs) is now established within evolutionary biology (5-7). IGEs are known to readily alter the evolutionary predictions of standard quantitative genetic models incorporating only direct genetic ...
The evolutionary theory of senescence underpins research in life history 9 evolution and the biology of aging. In 1957 G.C. Williams predicted that higher 10 adult death rates select for earlier senescence and shorter length of life, but pre-11 adult mortality doesn't matter to evolution. This was subsequently interpreted as 12 predicting that senescence should be caused by 'extrinsic' sources of mortality. 13 This idea still motivates empirical studies, even though formal, mathematical 14 theory shows it is wrong. It has nonetheless prospered because it offers an 15 intuitive explanation for patterns observed in nature. We review the flaws in 16Williams' model, explore alternative explanations for comparative patterns that 17 are consistent with the evolutionary theory of senescence and discuss how 18 hypotheses based upon it can be tested. We argue that focussing on how sources 19 of mortality affect ages differently offers greater insight into evolutionary 20 processes. 21
The Industrial Revolution and the accompanying nutritional, epidemiological and demographic transitions have profoundly changed human ecology and biology, leading to major shifts in life history traits, which include age and size at maturity, age-specific fertility and lifespan. Mismatch between past adaptations and the current environment means that gene variants linked to higher fitness in the past may now, through antagonistic pleiotropic effects, predispose post-transition populations to non-communicable diseases, such as Alzheimer disease, cancer and coronary artery disease. Increasing evidence suggests that the transition to modernity has also altered the direction and intensity of natural selection acting on many traits, with important implications for public and global health.
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