The Mechanisms of Senescence in Wild European Badgers
Date: 31 October 2014
Thesis or dissertation
University of Exeter
PhD in Biological Sciences
Overwhelming evidence for senescence, the within-individual decline in performance at advanced age, has now been documented in the natural populations of many taxa. As such, the focus of senescence research is shifting from simply documenting its existence, towards understanding the fundamental mechanisms underpinning it and determining ...
Overwhelming evidence for senescence, the within-individual decline in performance at advanced age, has now been documented in the natural populations of many taxa. As such, the focus of senescence research is shifting from simply documenting its existence, towards understanding the fundamental mechanisms underpinning it and determining which environmental factors give rise to the considerable variation in senescence rates observed in nature. In this thesis I use a wild population of European badgers (Meles meles) to investigate three important traits implicated in, or arising as a direct product of, senescence; immune cell telomere length, pro-inflammatory cytokine response and body mass declines in late life. My work reveals rare longitudinal evidence for the existence of senescence in immune traits in a wild mammal. First, I show that within-individual declines in immune cell telomere length occur with increasing age (Chapter 2). Second, after demonstrating that immune cell telomere length displays repeatable between-individual differences in adulthood, I show that the environmental conditions experienced in early-life contribute to such between-individual variation. Individuals that experienced harsh early-life environmental conditions had shorter immune cell telomere lengths than those that experienced favourable conditions (Chapter 3). Third, I show that within-individual declines in a second immune trait, pro-inflammatory cytokine response, also occur with age (Chapter 4). However, the declines in immune cell telomere length and pro-inflammatory cytokine response occur independently of one another (Chapter 4). Finally I take advantage of a 37 year longitudinal dataset to reveal that sex differences in body mass senescence arise as a consequence of the scale of intra-sexual competition experienced in early adulthood (Chapter 5). Taken together this work provides novel evidence suggesting that age-related declines in immunocompetence can contribute to whole organism senescence in the wild. Furthermore, evidence that early life environmental and social conditions can markedly influence senescence rates has important implications for our understanding of the drivers of variation in senescence rates observed within natural populations.
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