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D E Promislow

Publications and source records attributed to D E Promislow.

13 recordsLinked to original sources
PubMed2000

Age-specific effects of novel mutations in Drosophila melanogaster II. Fecundity and male mating ability.

Evolutionary theories of senescence assume that mutations with age-specific effects exist, yet until now, there has been little experimental evidence to support this assumption. In this study, we allowed mutations to accumulate in an outbred, wild population of Drosophila melanogaster to test for age-specific differences in both male mating ability and fecundity. We assayed for age-specific effects of mutations after 10, 20, and 30 generations of mutation accumulation. For mating ability, we found the strongest effects of mutations in the first half of the life span after 20 generations, and at nearly all ages by generation 30. These results are qualitatively consistent with results from a companion study in which age-specific mortality was assayed on the same lines of D. melanogaster. By contrast, effects of fecundity were confined to late ages after 20 generations of mutation accumulation, but by generation 30, as with male mating ability, effects of novel mutations were distributed across all age classes. We discuss several possible explanations for the differences that we observe between generations within traits, and among traits, and the relevance for these patterns to models of aging as well as models of mate choice and sexual selection.

Aging↗
PubMed2000

Age-specific effects of novel mutations in Drosophila melanogaster I. Mortality.

Theories for the evolution of aging rest on the assumption that at least some deleterious mutations have effects that are limited to certain ages. Many mutation accumulation studies have tried to measure the number and magnitude of deleterious mutations, but few studies have tried to determine the extent to which the effects of mutations are limited to particular ages. Here we estimate the age-specific effect of deleterious mutations on mortality rate in an outbred population of the fruit fly, Drosophila melanogaster. We used the 'middle class neighborhood' approach to accumulation mutations in populations of flies that had recently been obtained from the wild. There are mutations that increase mortality rates, but whose effects are limited to specific ages. The age-specificity of mutational effects differs between the sexes, between virgin and mated flies, and over time. After 10 and 20 generations of mutation accumulation, there were clear age-specific effects of mutations. After 30 generations, however, the degree of age-specificity decreased. In addition, mutation accumulation led to a steady increase in larval mortality and a small but significant increase in the sex ratio of eclosing flies. We discuss the implications of these results for models of aging, and suggest approaches that future studies should take to obtain accurate information on the age-specificity of novel mutations.

Aging↗
PubMed1999

Genomic demography: a life-history analysis of transposable element evolution.

Retrotransposons are ubiquitous mobile genetic elements that have played a significant role in shaping eukaryotic genome evolution. The genome of the yeast Saccharomyces cerevisiae harbours five families of retrotransposons, Ty1-Ty5. With the publication of the S. cerevisiae genome sequence, for the first time a full genomic complement of retrotransposon sequences is available. Analysis of these sequences promises to yield insight into the nature of host--transposon coevolution. Evolutionary change in Ty elements depends on their replication and excision rates, which have been determined in the laboratory. Rates measured in the laboratory may differ from those that have operated over evolutionary time. Based on an analysis of sequence data for the Ty1, Ty2 and hybrid Ty1/2 families, we develop a novel 'genomic demography' model to estimate long-term transposition and excision rates and to estimate how long ago these elements entered the yeast genome. We find that rates of excision and transposition have averaged 7.2-8.7 x 10(-8) per generation over evolutionary time. Two separate models provide upper- and lower-bound estimates for the age of the system, suggesting that the first elements entered the genome between approximately 50 million and 250 million generations ago.

Evolution, Molecular↗
PubMed1999

Toward reconciling inferences concerning genetic variation in senescence in Drosophila melanogaster.

Standard models for senescence predict an increase in the additive genetic variance for log mortality rate late in the life cycle. Variance component analysis of age-specific mortality rates of related cohorts is problematic. The actual mortality rates are not observable and can be estimated only crudely at early ages when few individuals are dying and at late ages when most are dead. Therefore, standard quantitative genetic analysis techniques cannot be applied with confidence. We present a novel and rigorous analysis that treats the mortality rates as missing data following two different parametric senescence models. Two recent studies of Drosophila melanogaster, the original analyses of which reached different conclusions, are reanalyzed here. The two-parameter Gompertz model assumes that mortality rates increase exponentially with age. A related but more complex three-parameter logistic model allows for subsequent leveling off in mortality rates at late ages. We find that while additive variance for mortality rates increases for late ages under the Gompertz model, it declines under the logistic model. The results from the two studies are similar, with differences attributable to differences between the experiments.

Aging↗
PubMed1998

Adult fitness consequences of sexual selection in Drosophila melanogaster.

Few experiments have demonstrated a genetic correlation between the process of sexual selection and fitness benefits in offspring, either through female choice or male competition. Those that have looked at the relationship between female choice and offspring fitness have focused on juvenile fitness components, rather than fitness at later stages in the life cycle. In addition, many of these studies have not controlled for possible maternal effects. To test for a relationship between sexual selection and adult fitness, we carried out an artificial selection experiment in the fruit fly, Drosophila melanogaster. We created two treatments that varied in the level of opportunity for sexual selection. Increased opportunity for female choice and male competition was genetically correlated with an increase in adult survivorship, as well as an increase in male and female body size. Contrary to previous, single-generation studies, we did not find an increase in larval competitive ability. This study demonstrates that mate choice and/or male-male competition are correlated with an increase in at least one adult fitness component of offspring.

Aging↗
PubMed1998

Mutation and senescence: where genetics and demography meet.

Two evolutionary genetic models-mutation accumulation and antagonistic pleiotropy-have been proposed to explain the origin and maintenance of senescence. In this paper, we focus our attention on the mutation accumulation model. We re-examine previous evidence for mutation accumulation in light of new information from large-scale demographic experiments. After discussing evidence for the predictions that have been put forth from models of mutation accumulation, we discuss two critical issues at length. First, we discuss the possibility that classical fruit fly stock maintenance regimes may give rise to spurious results in selection studies of aging. Second, we consider evidence for the assumptions underlying evolutionary models of aging. These models assume that mutations act additively on age-specific survival rate, that there exist mutations whose effects are confined to late age-classes, and that all mutations have equal effects. Recent empirical evidence suggests that each of these three assumptions is unlikely to be true. On the basis of these results, we do not conclude that mutation accumulation is no longer a valid explanation for the evolution of aging. Rather, we suggest that we now need to begin developing more biologically realistic genetic models for the evolution of aging.

Aging↗
PubMed1996

Age-specific patterns of genetic variance in Drosophila melanogaster. I. Mortality.

PETER MEDAWAR proposed that senescence arises from an age-related decline in the force of selection, which allows late-acting deleterious mutations to accumulate. Subsequent workers have suggested that mutation accumulation could produce an age-related increase in additive genetic variance (VA) for fitness traits, as recently found in Drosophila melanogaster. Here we report results from a genetic analysis of mortality in 65,134 D. melanogaster. Additive genetic variance for female mortality rates increases from 0.007 in the first week of life to 0.325 by the third week, and then declines to 0.002 by the seventh week. Males show a similar pattern, though total variance is lower than in females. In contrast to a predicted divergence in mortality curves, mortality curves of different genotypes are roughly parallel. Using a three-parameter model, we find significant VA for the slope and constant term of the curve describing age-specific mortality rates, and also for the rate at which mortality decelerates late in life. These results fail to support a prediction derived from MEDAWAR's "mutation accumulation" theory for the evolution of senescence. However, our results could be consistent with alternative interpretations of evolutionary models of aging.

Aging↗
PubMed1996

Age-specific patterns of genetic variance in Drosophila melanogaster. II. Fecundity and its genetic covariance with age-specific mortality.

Under the mutation accumulation model of senescence, it was predicted that the additive genetic variance (VA) for fitness traits will increase with age. We measured age-specific mortality and fecundity from 65,134 Drosophila melanogaster and estimated genetic variance components, based on reciprocal crosses of extracted second chromosome lines. Elsewhere we report the results for mortality. Here, for fecundity, we report a bimodal pattern for VA with peaks at 3 days and at 17-31 days. Under the antagonistic pleiotropy model of senescence, it was predicted that negative correlations will exist between early and late life history traits. For fecundity itself we find positive genetic correlations among age classes > 3 days but negative nonsignificant correlations between fecundity at 3 days and at older age classes. For fecundity vs. age-specific mortality, we find positive fitness correlations (negative genetic correlations) among the traits at all ages > 3 days but a negative fitness correlation between fecundity at 3 days and mortality at the oldest ages (positive genetic correlations). For age-specific mortality itself we find overwhelmingly positive genetic correlations among all age classes. The data suggest that mutation accumulation may be a major source of standing genetic variance for senescence.

Aging↗
PubMed1995

Genetic variation and aging.

Life span is subject to genetic modification in yeasts, nematodes, fruit flies, mice, humans, and other vertebrates and invertebrates. There are a few single-gene mutants known that extend life span in yeast and nematodes; in other experimental systems the character is treated quantitatively, and generally has a low to moderate heritability. Life span responds to artificial selection in Drosophila and Caenorhabditis. There are many candidate genes presently under investigation, including the anti-oxidizing enzymes and heat-shock proteins. The main evolutionary models of senescence are antagonistic pleiotropy and mutation accumulation, neither of which has substantial experimental support. The incorporation of analytical techniques from demography is playing an increasing role in research on aging.

Aging↗
PubMed1994

DNA repair and the evolution of longevity: a critical analysis.

Comparative gerontologists argue that variation among species in DNA repair rates may explain differences in maximum lifespan, and support this claim with the observation that DNA repair rates and lifespan correlate positively among mammals. However, these findings may be confounded by both size and phylogeny. Repair rates and lifespan may be positively correlated because both are positively correlated with body size. In addition, previous comparative studies have not controlled for the potentially confounding effects of phylogeny. In this study, I elucidate why we might expect larger species to have higher DNA repair rates, independent of differences in lifespan, and use existing data to test whether the relationship between DNA repair rates and lifespan holds up after controlling for the potentially confounding effects of size and phylogeny. Reanalysis of the existing data suggests that there is little comparative evidence in favour of the hypothesis relating DNA repair rates and lifespan.

Animals↗
PubMedDate not supplied

Age-specific fitness components in hybrid females of Drosophila pseudoobscura and D. persimilis.

Most models of hybridization assume that hybrids are less fit than their parental taxa. In contrast, some researchers have explored the possibility that hybrid individuals may actually have higher fitness and so play an important role in the generation of new species or adaptations. By estimating age-specific fitness components, we can determine not only how hybrid fitness differs from parental taxa, but also whether the fitness of hybrids relative to parental taxa changes with age. Here we describe an analysis of age-specific fitness traits in two species of Drosophila, D. pseudoobscura and D. persimilis, and their F1 hybrids. At early ages, hybrid females lay as many eggs as parental individuals, on average, but produce far fewer offspring. By late ages, in contrast, parental taxa show a steep decline in production not seen in hybrids, such that hybrids produce more offspring, on average, than parental taxa. Furthermore, egg-adult survival in hybrids is negatively correlated with egg density, whereas these traits are only weakly correlated in parental taxa. The results are limited somewhat by the fact that we analyze only two strains, and that these may be partially inbred. Nonetheless, the results are certainly illustrative, pointing out not only that at least some hybrid individuals may be as fit or fitter than parental taxa, but also that the difference between hybrids and parental taxa varies with age.

Age Factors↗