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J W Curtsinger

Publications and source records attributed to J W Curtsinger.

At least 19 recordsLinked to original sources
PubMed1997

Heat-induced longevity extension in Drosophila. I. Heat treatment, mortality, and thermotolerance.

Survival data were collected on a total of 28,000 Drosophila melanogaster adults in order to investigate mortality patterns and induced physiological responses after a mild thermal stress. A brief, nonlethal heat treatment extends adult life span at normal temperatures by an average of 2 days (64), compared to nontreated controls of the same genotypes. Life expectancy is extended as a demographic consequence of reduced age-specific mortality over a period of up to several weeks after the heat treatment. Heat treatment also increases tolerance to subsequent, more severe thermal stress. Observations on single-sex populations suggest that heat-induced longevity extension is independent of the suppression of reproductive activity.

Acclimatization↗
PubMed1996

Effect of density on age-specific mortality in Drosophila: a density supplementation experiment.

Age-specific mortality rates were studied at two adult density levels in four inbred lines of Drosophila melanogaster. In experimental populations, adult densities were maintained at constant levels throughout the experiment by replacing dead flies with live, marked mutants. In control populations, densities declined naturally as the cohorts aged. For all experimental populations the best mortality model is the two-stage Gompertz model, with slower mortality acceleration at older ages. Flies in the experimental populations generally lived longer than flies in control populations, regardless of sex, genotype, or initial density level. The data demonstrate that deceleration of age-specific mortality rates at older ages is not caused by declining cohort densities. Mortality deceleration is a real phenomenon that raises serious questions about the evolution of senescence.

Age Factors↗
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

Density and age-specific mortality.

Age-specific mortality rates decelerate at older ages in laboratory populations in the Medfly Ceratitis capitata. This has been interpreted by Carey et al. (1992) to reflect a slowing of the aging process, but might also be explained by declining adult density. Here it is argued that the density explanation, as presented by Graves and Mueller (1993), is unpersuasive for several reasons: extrapolations from Drosophila to Medflies are unjustified; the range of densities they studied is 2-120 times higher than that used in other studies; they ignore data on Medflies held in isolation, which rule out density effects; their own data suggest that initial cohort density has no effect on mortality rates at older ages, which is the relevant part of the life cycle; their experiment is too small to provide accurate estimates of mortality; new Medfly experiments executed at multiple densities show decelerating and then declining mortality rates at advanced ages for all densities. When Drosophila survivorship experiments are done on a sufficiently large scale they also show a deceleration of mortality at older ages that is not attributable to density effects. The deceleration of mortality rates is most likely a real facet of aging, and will have to be taken into consideration in any synthesis of the genetics and evolution of aging.

Aging↗
PubMed1995

Effect of adult cohort density on age-specific mortality in Drosophila melanogaster.

Mortality rates decelerate at older ages in experimental populations of Drosophila. It is unclear whether this reflects a real slow-down in the aging process, or an artifact of declining density. Mortality was studied in age-synchronized cohorts of four inbred lines at three initial densities that varied 10-fold. A total of 70,000 flies of both sexes were studied. There were large line x density, line, and sex effects, but no systematic relationship between density and life span was detected. Mortality curves level off at older ages in 23 out of 24 sex-genotype combinations, irrespective of initial cohort density. Density has only second-order effects on the pattern of oldest-old mortality over the range of densities studied here. The dramatic departure from Gompertz-type mortality dynamics at older ages is not an artifact of declining density in Drosophila.

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↗
PubMed1995

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.

Animals↗
PubMed1995

Survival curves subjected to occasional insults.

We describe a parametric family of survival curves which can be used to model time to event data in systems subjected to occasional insults or shocks. Parameters control the location, magnitude, and duration of the effect for each insult. We use these models to describe the survival history of a large cohort of Drosophila that were transferred to new vials on a weekly basis as their nutrient medium deteriorated. A periodic model with fewer parameters exhibits a good fit to the data.

Animals↗
PubMed1994

Piecewise exponential survival curves with smooth transitions.

Several models of a population survival curve composed of two piecewise exponential distributions are developed. In one formulation the hazard rate changes at a point that is an unobservable random variable that varies between individuals. The population hazard function may decrease with age even when all individuals' hazards are increasing. In a second formulation, the population hazard function is modeled directly. Several models are fit to the survival history of a cohort of 5751 highly inbred male Drosophila melanogaster and the British coal mining disaster data.

Animals↗
PubMed1992

Demography of genotypes: failure of the limited life-span paradigm in Drosophila melanogaster.

Experimental systems that are amenable to genetic manipulation can be used to address fundamental questions about genetic and nongenetic determinants of longevity. Analysis of large cohorts of ten genotypes of Drosophila melanogaster raised under conditions that favored extended survival has revealed variation between genotypes in both the slope and location of age-specific mortality curves. More detailed examination of a single genotype showed that the mortality trajectory was best fit by a two-stage Gompertz model, with no age-specific increase in mortality rates beyond 30 days after emergence. These results are contrary to the limited life-span paradigm, which postulates well-defined, genotype-specific limits on life-span and brief periods of intense and rapidly accelerating mortality rates at the oldest age.

Aging↗
PubMed1990

Genotype and anesthetic determine mate choice in Drosophila melanogaster.

Genetic differences that influence mating preferences were studied in genetically defined lines of Drosophila melanogaster. Initial results suggested substantial differences between two types of females with respect to the types of male preferred as mates, but further experimentation showed that the mating patterns were conditional on the mode of anesthesia (CO2 versus ether). In a statistical test of independence, the major determinant of mating choice in these experiments was due to an interaction effect between genotypes and mode of anesthesia. The observations might be explained by the differential sensitivity of male genotypes to ether. Etherization at emergence has lasting effects on mating behavior; it alters not only the latency and frequency of mating 4 days later, but also the pattern of matings observed.

Animals↗
PubMed1986

Relationship between alpha-glycerophosphate dehydrogenase activity and metabolic rate during flight in Drosophila melanogaster.

Measurements of wing-beat frequency (WBF) have been used to characterize flight muscle metabolic rate in Drosophila melanogaster during tethered flight. Progeny of crosses between 17 X-chromosome substitution lines and three null-activity stocks have been studied in order to determine the effect on flight metabolism of sharply reduced activity of alpha-glycerophosphate dehydrogenase (alpha GPDH). It was found that flies with an approximate 50% reduction in alpha GPDH activity have a metabolic rate that is, in most cases, indistinguishable from that of wild-type flies and, in the most extreme cases, reduced by only 4%. These results demonstrate that alpha Gpdh is not a "major gene" for flight metabolism, in the quantitative genetic sense of the term. These results are in agreement with the Kacser and Burns (1973, 1979, 1981) theory of flux, which postulates that the activity of an enzyme embedded in a multienzyme pathway can sometimes vary from wild-type to very low levels (perhaps 5-10% wild type) with no significant effect on flux through the total pathway.

Alleles↗
PubMed1985

Genetic variability of flight metabolism in Drosophila melanogaster. II. Relationship between power output and enzyme activity levels.

The major goal of the studies reported here was to determine the extent to which genetic variation in the activities of the enzymes participating in flight metabolism contributes to variation in the mechanical power output of the flight muscles in Drosophila melanogaster. Isogenic chromosome substitution lines were used to partition the variance of both types of quantitative trait into genetic and environmental components. The mechanical power output was estimated from the wingbeat frequency, wing amplitude and wing morphology of tethered flies by applying the aerodynamic models of Weis-Fogh and Ellington. There were three major results. (1) Chromosomes sampled from natural populations provide a large and repeatable genetic component to the variation in the activities of most of the 15 flight metabolism enzymes investigated and to the variation in the mechanical power output of the flight muscles. (2) The mechanical power output is a sensitive indicator of the rate of flight metabolism (i.e., rate of oxygen consumption during tethered flight). (3) In spite of (1) and (2), no convincing cases of individual enzyme effects on power output were detected, although the number and sign of the significant enzyme-power correlations suggests that such effects are not totally lacking.

Animals↗
PubMed1984

Components of selection in X chromosome lines of Drosophila melanogaster: sex ratio modification by meiotic drive and viability selection.

Selection coefficients and segregation parameters have been estimated in 18 randomly chosen lines carrying wild X chromosomes on the cn bw genetic background. Each line was studied in replicated crosses of four types, with approximately 100 replications per line per cross. Crosses in which male X chromosomes differed exhibited significant sex ratio heterogeneity. Maximum likelihood estimation of segregation parameters revealed two lines in which the proportion of X-bearing gametes produced by males was significantly different from Mendelian expectations. These observations suggest that segregation distortion is a common feature of naturally occurring genetic variation. Non-Mendelian segregation has important evolutionary implications.

Animals↗
PubMed1983

A two-generation study of human sex-ratio variation.

We report here the first vertical population study of human sex-ratio variation. Sex-ratio data for 2 generations from Akita, Japan, have been analyzed. Parental age, birth order, sequences of the sexes at birth, and generations have no statistically significant effect on sex ratio. There is a slight excess of males at birth, as is typical for human sex-ratio studies. There is evidence of sex-ratio-dependent family planning. An analysis of vertical transmission of sex-ratio modifying factors that excludes effects of birth order in both the parental and offspring generations has detected a marginally significant paternal effect. Genetic variability of the sex ratio, if present at all, is of a very minor magnitude.

Adult↗
PubMed1982

Naturally occurring enzyme activity variation in Drosophila melanogaster. I. Sources of variation for 23 enzymes.

The genetic component of variation of enzyme activity levels in Drosophila melanogaster was investigated by using 48 second- and 48 third-chromosome isogenic substitution lines derived from natural populations. The results confirm those of our earlier experiments with the same lines and extend them to a number of additional enzymes. All 23 enzymes show a significant genetic component to the variation in one or both sets of lines and only a small part of this variation is accounted for by variation among the lines in the amount of tissue per fly. The magnitude of line effects is, in most cases, considerably larger than the magnitude of environmental and measurement error effects, and the line effects are approximately continuous in distribution. Variation in the geographic origin and karyotype of the chromosomes generally does not contribute to the line component of variation, but allozymes provide an important source of variation for a few of the enzymes. Many of the enzymes show evidence for variation of activity modifiers that are not linked to the structural locus of the enzyme.

Animals↗