Despite extensive evidence of senescence, the decline in performance with age, in wild populations, the drivers ofindividual variation in senescence patternsare still unresolved. In this thesis,I study how early-life environmental, genetic and transgenerational effects contribute to individual variation in senescence patterns, using telomere dynamics,ina wild population ofEuropean badgers (Meles meles).I discovered that telomere length forms a complex relationship with age,withboth decreases and increases in telomere length that cannot be fully explained by measurement error. Telomere length was not sex-specific, but early-life telomere length predicts survival to adulthood (>1 year old) and lifespan. Within-individual changes in telomere length could be due to age-related changesin leukocyte cell composition in response to social conditions. While variation in (early-life)telomere length was associatedwith the abundance and variation in food availability, andnatal but not adultsocial conditions, I found no evidence for heritability of telomere length or transgenerationaleffects, through parental age at conceptioneffects. Additionally, individuals experiencingmatching early-and later-life conditions had longer lifespans,even though there was only moderate autocorrelation in environmental quality, but this also depended on the mean environmental qualityacross adulthood. Ialsodeveloped a novel approach to the analysis of long-term studies, termed slicing, which overcomes problems with confounding effects and cross-classified data structures.My research shows that individual variation in telomere length and senescence is a consequence of early-life environmental, not genetic or transgenerational, effects in European badgers. In addition, I show the potential for adaptive responses in anticipation of the adult environment and the importance ofstudying both the mean of and variability in early-life conditions to fully understand the selective pressures on senescence.
|Status||Published - 2020|