Abstracts (first author)
Genetic basis of ageing evolution under differential extrinsic mortality in a nematode
Ageing is inevitable in most living organisms but how ageing evolves is unclear. Because of extrinsic mortality due to a variety of biotic and abiotic factors, the strength of selection declines with age. This “selection shadow” may result in the accumulation of detrimental mutations with late-life expression or fixation of antagonistically pleiotropic mutations that increase fitness in early-life at the expense of fitness in late-life. Classic theory has thus predicted that if mortality is high, the evolutionary contribution of old individuals will be low and that this will lead to evolution of accelerated ageing and decreased longevity. However, if mortality is non-random, condition-dependent selection is likely to yield individuals with strong resistance to typical causes of mortality. Emerging theory thus suggests that condition-dependence may alter, and even reverse, the classic pattern. We have previously employed an experimental evolution design, using a nematode worm Caenorhabditis remanei, that allowed us to disentangle the effects of mortality rate (high vs low) and mortality source (random vs heat-shock) on the evolution of longevity. We observed the evolution of reduced longevity under high random mortality, confirming the classic prediction. In contrast, high condition-dependent mortality led to the evolution of increased longevity and lower late-life mortality rates, supporting a key role for mortality source in the evolution of ageing. In the present project, we examine which genes underlie the evolution of lifespan by quantifying divergences in gene expression across our selection lines. Using RNA sequencing, we quantified the differentially expressed genes in young and old nematodes from the four selection regimes. The results will be discussed.