Abstract
Telomeres, the caps of eukaryotic chromosomes, control chromosome stability and cellular senescence, but aging and exposure to chronic stress are suspected to cause attrition of telomere length. We investigated the effect of social isolation on telomere length in the highly social and intelligent African Grey parrot (Psittacus erithacus erithacus). Our study population consisted of single-housed (n = 26) and pair-housed (n = 19) captive individuals between 0.75 to 45 years of age. Relative telomere length of erythrocyte DNA was measured by quantitative real-time PCR. We found that telomere length declined with age (p<0.001), and socially isolated parrots had significantly shorter telomeres compared to pair-housed birds (p<0.001) – even among birds of similar ages. Our findings provide the first evidence that social isolation affects telomere length, which supports the hypothesis that telomeres provide a biomarker indicating exposure to chronic stress.
Highlights
Individual variation in ageing and health are associated with differences in telomere length (TL) [1]
Relative telomere length (RTL) declined with age (n = 45; generalized additive model (GAM), p,0.001), and single-housed birds had shorter telomeres compared to the group of pair-housed individuals
Using the Cox proportional hazard model we found a positive but non-significant effect of age on mortality (b = 0.109; standard error (SE) = 0.72; p = 0.129) and a negative, and non-significant effect of RTL on mortality (b = 214.918; SE = 10.331; p = 0.149). (Data for this study are available upon request from the corresponding author)
Summary
Individual variation in ageing and health are associated with differences in telomere length (TL) [1]. Telomeres are specialized protein-DNA complexes, which provide a protective cap on the end of linear chromosomes and prevent chromosomal degradation and end-to-end fusions by ‘hiding’ free DNA ends. In vitro studies show that telomeres become shorter with every cell division due to the inability of DNA polymerase to fully replicate the 59end of linear DNA (‘end-replication problem’). The causes of variation in telomere shortening (and repair) among individuals are not fully understood, though the leading hypothesis suggests they are due to differences in exposure to chronic stress and lifestyle [1,11,12]
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