Mortality Plateaus and the Evolution of Senescence: Why are Old-Age Mortality Rates so Low?

Pletcher, Scott D.; Curtsinger, James W.

doi:10.2307/2411081

Cited by 86 publications

(72 citation statements)

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“…Among the pooled outbred lines, there is little evidence of deceleration (Figure 1, inset), although there does appear to be some deceleration among inbred lines. In contrast to previous studies with laboratory lines (eg, Pletcher and Curtsinger, 1998), late-age mortality rates are relatively high, with m x between 0.3 and 0.5 (-1.2 to -0.7 on a natural log scale) (Figure 1).…”

Section: Resultscontrasting

confidence: 86%

Quantitative genetic tests of recent senescence theory: age-specific mortality and male fertility in Drosophila melanogaster

Snoke

Promislow

2003

Heredity

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Quantitative genetic models of aging predict that additive genetic variance for fitness components should increase with age. However, recent studies have found that at very late ages, the genetic variance components decline. This decline may be due to an age-related drop in reproductive effort. If genetic variance in reproductive effort affects the genetic variance in mortality, the decline in reproductive effort at late ages should lead to a decrease in the genetic variance in mortality. To test this, we carried out a large-scale quantitative genetic analysis of age-specific mortality and fertility in virgin male Drosophila melanogaster. As in earlier studies, we found that the additive variance for age-specific mortality and fertility declined at late ages. Also, recent theoretical developments provide new predictions to distinguish between the mutation accumulation (MA) and antagonistic pleiotropy (AP) models of senescence. The deleterious effects of inbreeding are expected to increase with age under MA, but not under AP. This prediction was supported for both age-specific mortality and male fertility. Under AP, the ratio of dominance to additive variance is expected to decline with age. This predicition, too, was supported by the data analyzed here. Taken together, these analyses provide support for both the models playing a role in the aging process. We argue that the time has come to move beyond a simple comparison of these genetic models, and to think more deeply about the evolutionary causes and consequences of senescence.

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Section: Resultscontrasting

confidence: 86%

Quantitative genetic tests of recent senescence theory: age-specific mortality and male fertility in Drosophila melanogaster

Snoke

Promislow

2003

Heredity

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“…Instead, the rate of increase in mortality quickly decelerated and reached a plateau, as observed in many other studies (Carey et al 1992;Mueller and Rose 1996;Pletcher and Curtsinger 1998;Wachter 1999) and observed previously for both C. maculatus and S. limbatus (Fox and Moya-Laraño 2003;Fox et al 2003bFox et al , 2004a. This deceleration in the rate of increase in mortality reduced the relative difference between inbred and outbred beetles, reducing the estimated inbreeding load at older ages.…”

Section: Discussionsupporting

confidence: 75%

“…This model is similar to a Gompertz mortality model except that it incorporates a term, s, to account for the slowing of the increase in mortality rate with age (Pletcher and Curtsinger 1998); when s ¼ 0 the logistic model reduces to the Gompertz model. Both a Gompertz model and a Gompertz-Makeham model provided significantly worse fits to the data (in all analyses) than did the logistic model.…”

Section: Methodsmentioning

confidence: 99%

The Genetic Architecture of Life Span and Mortality Rates: Gender and Species Differences in Inbreeding Load of Two Seed-Feeding Beetles

et al. 2006

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We examine the inbreeding load for adult life span and mortality rates of two seed beetle species, Callosobruchus maculatus and Stator limbatus. Inbreeding load differs substantially between males and females in both study populations of C. maculatus-life span of inbred females was 9-13% shorter than the life span of outbred females, whereas the life span of inbred males did not differ from the life span of outbred males. The effect of inbreeding on female life span was largely due to an increase in the slope of the mortality curve. In contrast, inbreeding had only a small effect on the life span of S. limbatus-life spans of inbred beetles were $5% shorter than those of outbred beetles, and there was no difference in inbreeding load between the sexes. The inbreeding load for mean life span was $0.4-0.6 lethal equivalents per haploid gamete for female C. maculatus and $0.2-0.3 for both males and females of S. limbatus, all within the range of estimates commonly obtained for Drosophila. However, contrary to the predictions of mutation-accumulation models, inbreeding load for loci affecting mortality rates did not increase with age in either species, despite an effect of inbreeding on the initial rate of increase in mortality. This was because mortality rates decelerated with age and converged to a mortality plateau for both outbred and inbred beetles.T HE evolution of life span, mortality rates, and patterns of senescence is of substantial interest because there is tremendous variation in these traits at all taxonomic levels (Promislow 1991) and because of the medical implications of understanding the genetics underlying mortality rates. Studies on mice, Drosophila, and Caenorhabditis elegans have identified numerous genes that influence life span and/or rates of senescence (Harshman 2002). Recent studies of life span in Drosophila melanogaster indicate that inheritance of life span can be quite complex, with both dominance and epistasis having significant effects on variation in life span (Harshman 2002;Leips and Mackay 2002;Mackay 2002;Spencer et al. 2003;Spencer and Promislow 2005). These studies also show that the genetic architecture (number of genes and degree of allelic and genic interactions) underlying life span differs between the sexes and depends on the environmental conditions in which individuals are reared.One of the major genetic mechanisms proposed to underlie senescence is the accumulation in populations of late-acting deleterious alleles due to the declining force of selection with increasing age (mutation-accumulation theory) (Hughes and Reynolds 2005). Research has now identified many genes and chromosomal regions (QTL) that affect life span in model organisms but we have few data on the frequency of deleterious alleles affecting life span (De Luca et al. 2003;Carbone et al. 2006). We have less data on the sources of variation in deleterious alleles and the age specificity of expression of those alleles and thus their effects on age-specific mortality rates.Inbreeding studies are a com...

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“…Thus, differences in extrinsic mortality rates did lead to the evolution of the expected differences in intrinsic mortality rates. Recently, there has been considerable discussion (33)(34)(35)(36) about the shape of mortality curves, stimulated by the observation of decelerating mortalities late in life (37). In this study, female age-specific intrinsic mortality (d x ) stopped increasing after about 65 days of age, then decreased, then increased again (Fig.…”

Section: Resultsmentioning

confidence: 75%

Experimental evolution of aging, growth, and reproduction in fruitflies

Stearns

Ackermann²,

Doebeli³

et al. 2000

Proceedings of the National Academy of Sciences

199

127

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We report in this paper an evolutionary experiment on Drosophila that tested life-history theory and the evolutionary theory of aging. As theory predicts, higher extrinsic mortality rates did lead to the evolution of higher intrinsic mortality rates, to shorter lifespans, and to decreased age and size at eclosion; peak fecundity also shifted earlier in life. These results confirm the key role of extrinsic mortality rates in the evolution of growth, maturation, reproduction, and aging, and they do so with a selection regime that maintained selection on fertility throughout life while holding population densities constant.life-history evolution ͉ lifespan ͉ age at maturity ͉ body size ͉ Drosophila I n this paper, we report a case study in experimental evolution with the fruit fly Drosophila melanogaster that is designed to test predictions of life-history theory (1-6) and the evolutionary theory of aging (7-11). It did confirm those predictions. The change in the environment that drove phenotypic change was a difference in extrinsic adult mortality rates. What is different in this experiment is that mortality was applied in a way closely resembling natural conditions rather than by using traditional artificial selection. Treatments differed only in adult mortality applied twice each week, which maintained selection on fertility throughout life.Evolutionary Theory of Aging and Life Histories. Evolutionary theory predicts the impact of a difference in extrinsic mortality on intrinsic mortality rates (hence, lifespan) and on growth, maturation, body size, and reproduction. When extrinsic mortality rates increase, they lower the probability of survival to a given age and cause the strength of selection to decline faster with age, making an increase in intrinsic mortality rates with age ''more affordable'' or ''less avoidable.'' From this concept follows a central prediction of the evolutionary theory of aging (11): Higher extrinsic mortality rates should lead to higher intrinsic mortality rates and a decrease in lifespan, which is a prediction adumbrated by Weismann (7) and Medawar (8), explicit in the work of Williams (9), quantitative in the research of Hamilton (10) and Charlesworth (1), and consistent with comparative evidence (11-13).Extrinsic mortality rates also affect the evolution of other life-history traits. Higher extrinsic adult mortality rates should lead to higher reproductive effort early in life and, for age-but not stage-dependent life histories (5), to more rapid development and eclosion at an earlier age and a smaller size (1-6).Experimental Evolution and Artificial Selection. Recently, a new tool has been exploited to test such predictions: experimental evolution (14). In contrast to artificial selection, in which the experimenter determines which trait is selected, in experimental evolution, the experimenter creates the conditions under which a prediction should hold and lets the evolving population determine with which traits the problem will be solved. This approach has yielded important insigh...

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Mortality Plateaus and the Evolution of Senescence: Why are Old-Age Mortality Rates so Low?

Cited by 86 publications

References 0 publications

Quantitative genetic tests of recent senescence theory: age-specific mortality and male fertility in Drosophila melanogaster

Quantitative genetic tests of recent senescence theory: age-specific mortality and male fertility in Drosophila melanogaster

The Genetic Architecture of Life Span and Mortality Rates: Gender and Species Differences in Inbreeding Load of Two Seed-Feeding Beetles

Experimental evolution of aging, growth, and reproduction in fruitflies

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