Abstract
Senescence may evolve when genes have antagonistic effects between early reproduction and later age-specific mortality. Although widely consistent with data of quantitative genetics, this model has yet to be validated with the identification of a specific locus presenting such trade-offs. The molecular chaperone hsp70 may be a candidate for such a gene. Heat induced expression of the Hsp70 protein in adults decreases rates of age-specific mortality during normal aging, while maternally experienced heat shock depresses the production of mature progeny. Here we show that maternal heat shock reduces the proportion of egg hatch but not the viability of successfully hatched offspring. To assess whether heat induced maternal expression of hsp70 causes reduced egg hatch, we measured the proportion of eggs that hatch from females engineered to overexpress hsp70 transgenes. We used the same transgenic strains that extend longevity upon hsp70 expression and found that Hsp70 is sufficient to suppress egg hatch. The proportion of egg hatch as a function of hsp70 expression was not reduced in the first eggs laid after maternal heat shock, but appears in later laid eggs, which were at preoogenic and early vitellogenic stages during the maternal expression of hsp70. The contervailing effects of hsp70 upon fecundity and subsequent age-specific mortality exemplify antagonistic pleiotropy, and this trade-off could contribute to the evolution of Drosophila senescence.
