List of Accepted Abstracts

Evolutionary theory predicts a rapid decline in the strength of natural selection with ageing and it might become negligible after the prime reproductive age is passed. Natural selection that optimizes organismal physiology for development and reproduction early in life can become too weak to effectively regulate the late-life performances in older individuals. This hypothesis is perhaps consistent with our previous studies with insect models, where immune defense against pathogens turned progressively over-reactive and nonspecific with ageing, which in turn increased the immunopathological costs and post-infection mortality. Also, immunopathological costs of early-life immune activation in juveniles are often paid at later life-stages, leading to faster ageing and morbid phenotypes. However, there are no direct experiments to test how age-specific changes in immune responses in populations are associated with their intrinsic rate of ageing and concomitant weakening of selection pressure beyond the reproductive age. To fill this gap, we used replicated populations of the fruit fly Drosophila melanogaster with divergent reproductive schedules and thereby evolving different ageing rates (e.g. ‘early reproduction-faster ageing’ vs ‘late reproduction-delayed ageing’). We tracked the changes in their immunity and post-infection survival throughout their entire lifespan (i.e. starting from the day of eclosion to their reproductive window and then until the 90 percentiles of their total lifespan). We found that populations evolving with an early reproductive schedule and accelerated ageing rate also showed early onset of immune senescence, characterized by less effective immunity with higher bacterial load and post-infection mortality. Interestingly, populations evolving with delayed reproductive schedules and slower ageing rates had lower immunity and higher infection-related mortality at early stages of their adult lifespan. However, their ability to maintain a balanced immunity and post-infection health was maximised at their reproductive window and then declined rapidly thereafter. These results indicate that weaker selection strength post-reproductive prime can indeed be a plausible driver of both development and ageing of immunity at the population level, with strong implications to health and pathogenic infections.