The ecological genetics of senescence and stress resistance in Caenorhabditis elegans

Longevity and the rate of senescence are determined by the ecological conditions during a population's recent evolutionary history, and are intrinsically linked to other components of life history and to fitness. These traits should be examined in an ecological context, in which other aspects of the life history are taken into account. However, although many mutations which promote longevity in model organisms disrupt mechanisms that are involved in responding to environmental change, trade-offs associated with increased lifespan have typically been examined in benign laboratory conditions. In the nematode Caenorhabditis elegans, long-lived, stress resisitant age-1(hx546) mutants can compete with wild type worms in favourable growth conditions, but display fitness costs when populations are periodically starved. By monitoring termporal changes in genotype frequencies, I have established that age-1 mutants can have higher fitness that the wild type strain if mixed genotype populations are exposed to periods of thermal or oxidative stress when food is available. Genotype-by-environment interactions, and spatial and temporal distributions of the FOXO transcriptions factor DAF-16, suggest that this is because age-1 mutants are more able to survive, develop and reproduce during and/or after exposure to environmental stress, due to increased expression of genes involved in somatic maintenance and repair. Using population projection matrices, I have demonstrated that age-1(hx546) mutant allele can confer a selective advantage over the wild type genotype when populations experience abiotic stress, even if periods of starvation are frequently endured. This is the first demonstration that a long-lived, laboratory-derived mutant can have higher fitness that a wild type genotype under specific environmental conditions. The results imply that, is genetic variation is present in populations which encounter harsh conditions, increased longevity can evolve as a consequence of selection for greater resistance to stress. I have also established that the effects of mutations which promote longevity on the ability to tolerate environmental stress can be context dependent and that long-lived age-1(hx546) mutants display increased cold tolerance, relative to wild type worms, due to increased expression of ∆9 desaturase genes and additional transcriptional targets of DAF-16. The results presented in this theis suggests that genetic and life history responses to environmental stress deserve a more prominent role in evolutionary studies of aging.