An evolutionary heterogeneity model of late-life fecundity in Drosophila

Abstract

There is now a significant body of research that establishes the deceleration of mortality rates in late life and their ultimate leveling off on a late-life plateau. Natural selection has been offered as one mechanism responsible for these plateaus. The force of natural selection should also exert such effects on female fecundity. We have already developed a model of female fecundity in late life that incorporates the general predictions of the evolutionary model. The original evolutionary model predicts a decline in fecundity from a peak in early life, followed by a plateau with non-zero fecundity in late life. However, in Drosophila there is also a well-defined decline in fecundity among dying flies, here called the "death spiral". This effect produces heterogeneity between dying and non-dying flies. Here a hybrid evolutionary heterogeneity model is developed to accommodate both the evolutionary plateau prediction and the death spiral. It is shown that this evolutionary heterogeneity model gives a much better fit to late-life fecundity data.

Evolution of ageing since Darwin

“…Age-specific fecundity for two populations of D. melanogaster subject to different demographic selection regimes. Mean fecundity for the early reproducing ACO (circles) and late reproducing CO (triangles) females are shown along with a fitted regression (solid line) based on the evolutionary heterogeneity model of female fecundity (Mueller et al 2007). The estimated ages at which the fecundity plateaus begin are shown with arrows.…”

“…particular, evolutionary theory suggests that fecundity should plateau sometime after the last age of survival in a population's evolutionary history. In several independent experiments, Rauser et al (2003Rauser et al ( , 2006b and Mueller et al (2007) found late-life fecundity plateaus in populations of D. melanogaster. More notably, they found statistically significant differences in the days at which late-life fecundity plateaued in populations with different last ages of reproduction in their recent evolutionary history (figure 6; Rauser et al 2006b).…”

“…In any case, by 1984 the theoretical development of the evolutionary theory of ageing and its experimental corroboration were well in hand. Additional work is ongoing on the two key population genetic mechanisms for the evolution of ageing, antagonistic pleiotropy and mutation accumulation, a recent review of this work being that of Rose et al (2007). Both mechanisms appear to be involved, as these two mechanistic hypotheses are not mutually exclusive, although the evidence in favour of antagonistic pleiotropy as a genetic mechanism for the evolution of ageing has generally been clearer than that for mutation accumulation.…”

What is lifespan regulation and why does it exist?

“…In that regard, a relatively new demographic phenomenon has emerged; the rate of increase in death rates at older ages has slowed in developed countries. It has also been observed in non-human populations (Mueller et al 2007). This so-called ''mortality plateau'' is a violation of the invariant increase in death rates predicted by traditional models like the Gompertz.…”

Progress & Prospects: Gene therapy in aging

“…Some of the major factors comprising epigenetic modulators are prenatal maternal health, nutritional and hormonal status, and postnatal access to nutrition and exposure to viruses, bacteria and other germs, especially until and around the age of puberty. 17,[48][49][50][51] Therefore, an ideal strategy for the prevention or modulation of aging for extended health span incorporates genetic and epigenetic interventions. Defective or inefficient genetic pathways, which either lead to the emergence of specific diseases or significantly enhance the chances of a disease surely require successful application of the main stream gene therapy approaches including stem cells.…”