Scott D. Pletcher

Mortality plateaus and the evolution of senescence: Why are old-age mortality rates so low?

Age‐specific mortality rates level off far below 100% at advanced ages in experimental populations of Drosophila melanogaster and other organisms. This observation is inconsistent with the equilibrium predictions of both the antagonistic pleiotropy and mutation accumulation models of senescence, which, under a wide variety of assumptions, predict a “wall” of mortality rates near 100% at postreproductive ages. Previous models of age‐specific mortality patterns are discussed in light of recent demographic data concerning late‐age mortality deceleration and age‐specific properties of new mutations. The most recent theory (Mueller and Rose 1996) argues that existing evolutionary models can easily and robustly explain the demographic data. Here we discuss the sensitivity of that analysis to different types of mutational effects, and demonstrate that its conclusion is very sensitive to assumptions about mutations. A legitimate resolution of evolutionary theory and demographic data will require experimental observations on the age‐specificity of mutational effects for new mutations and the degree to which mortality rates in adjacent ages are constrained to be similar (positive pleiotropy), as well as consideration of redundancy and heterogeneity models from demographic theory.

The fractionation experiment: reducing heterogeneity to investigate age-specific mortality in Drosophila

Age-specific mortality rates decelerate at older ages in both genetically homogenous and heterogeneous populations of Drosophila. One explanation proposed for deceleration is population heterogeneity. This hypothesis suggests that a population consists of sub-populations that differ in mortality characteristics and that the deceleration is the result of selective survival of stronger individuals. Here we describe an experiment that fractionates populations into several sub-populations without changing the physiological characteristics of the post-fractionated populations. Through a careful process of selection of Drosophila eggs, larvae, pupae and adults, we attempt to reduce as much as possible the degree of pre-adult, environmentally induced heterogeneity among individuals of a genetically identical cohort. We then ask whether such cohorts, when compared to non-fractionated populations, exhibit a lesser degree of mortality deceleration at advanced ages. From a total of 106 fractionated and control populations, consisting of 51331 individuals, 101 populations (93% of the fractionated populations and 100% of the control populations) exhibit a significant amount of mortality deceleration late in life. These observations suggest that environmental heterogeneity accrued during larval development is not a major factor contributing to mortality deceleration at older ages.

The influence of environmentally induced heterogeneity on age-specific genetic variance for mortality rates

Using parametric models that describe the increase in mortality rates with age, we demonstrate that environmentally induced heterogeneity among genetically identical individuals is sufficient to generate biased estimates of age-specific genetic variance. Although the magnitude of the bias may change with age, one general trend emerges: the true genetic variance at the oldest ages is likely to be dramatically underestimated. Our results are robust to different manifestations of heterogeneity and suggest that such a bias is a general feature of these models. We note that age-dependent estimates of genetic variance for characters that are correlated with mortality (either genetically or environmentally) can be expected to be similarly affected. The results are independent of sample size and suggest that the bias may be more widespread in the literature than is currently appreciated. Our results are discussed with reference to existing data on mortality variance in Drosophila melanogaster.

Selection for Increased Longevity in Drosophila melanogaster: A Response to Baret and Lints

Baret and Lints [Gerontology 1993;39:252-259] have questioned the interpretation of artificial selection experiments for increased longevity in Drosophila. They suggest that such experiments cannot demonstrate the genetic determination of longevity, because line differences in mean longevity are confounded with erratic temporal variations in life span. Using 15,000 flies from selected and control lines developed by Luckinbill and Clare [Heredity 1985;55:9-19], we show here that when lines are tested simultaneously in a carefully controlled environment, they exhibit markedly different average life spans: selected males live 20 days longer than controls, and selected females live 10 days longer. These and other observations leave no doubt about the existence of heritable variation influencing longevity in Drosophila.

Mating behavior in Drosophila melanogaster selected for altered longevity

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Age-specific mortality costs of exposure to inbred Drosophila melanogaster in relation to longevity selection

This article address the hypotheses that selection for early- or late-life fitness changes patterns of reproductive behavior, that this behavior may be dependent on the genetic makeup of the females, and that patterns of male mortality are strongly dependent on the type of females to which they are exposed. Flies selected for late-life reproduction and their associated stocks selected for early reproduction were exposed to flies of the opposite sex from either the same stock or a highly inbred stock. Males of both long- and short-lived stocks showed an increase in early mortality when exposed to inbred females. In addition, when males were exposed to inbred females early in life they showed a lower age-specific mortality rate late in life than males exposed to females from their own stock. Interestingly, females exposed to inbred males showed a significant reduction in mean longevity. Analysis of age-specific mortality revealed that this reduction was brought about as a result of increased early mortality. Interpretation of the results from an analysis of mean longevity not only fails to identify important information--as shown from a demographic analysis of age-specific mortality--but also presents a misleading description of mortality costs.