Meeting Abstract
Both maternal stress exposure and stress exposure during development exert negative effects on the adult phenotype in a range of organisms. However, the mechanisms through which early life exposure to stressors is translated into impaired function in adulthood are unclear. One way in which conditions in the developmental environment may have systemic effects that are particularly evident late in life, and are associated with accelerated senescence, is through an elevated rate of telomere attrition. Telomere shortening is a normal part of cell division, but exposure to inflammation is hypothesized to accelerate the rate of loss. Thus, elevated levels of inflammation, particularly during development, should be associated with increased telomere attrition and reduced survival. Zebra finches (Taeniopygia guttata) exposed to an immune challenge during development that was not experienced by the mother prior to egg production, produce higher levels of corticosterone in response to stress in adulthood. Additionally, individuals with higher corticosterone levels have shorter lifespans in captivity. We will present data that test the hypothesis that immune activation during development induces increased telomere attrition. Telomere length and loss rate are related to survival, and the ability to minimize telomere loss and maximize lifespan, particularly in environments that induce higher rates of telomere loss, may be an important factor underlying life history trade-offs.
