The developmental conditions that an individual experiences have emerged as a major predictor for its adult condition. Accumulating evidence suggests that the footprint of challenging early developmental conditions is embedded in the length of telomeres –protective DNA sequences at the end of each chromosome - which shorten with progressing age and exposure to stress. Many mechanisms underlying telomere attrition, as well as the causal consequences for organisms, are still unresolved. One major phenomenon is the shortening effect that glucocorticoids exert on telomeres at different ontogenetic stages in both humans and animals. The aim of this study is to investigate the physiological routes by which glucocorticoids determine telomere dynamics during growth and the resulting fitness consequences. I am addressing this goal by relating mitochondrial function, gene expression, oxidative stress parameters and fitness-related traits to telomere length in wild birds having different life-history traits (i.e. songbirds and seabirds).
This paper shows that increased glucocorticoid concentrations in early life cause mitochondrial inefficiency and short telomeres in fast developing passerines.
Stefania Casagrande, Antoine Stier, Pat Monaghan, Jasmine Lopez Loveland, Winifred Boner, Sara Lupi, Rachele Trevisi, and Michaela Hau, "Increased glucocorticoid concentrations in early life cause mitochondrial inefficiency and short telomeres," The Journal of Experimental Biology 223 (15), jeb222513 (2020).
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Stress exposure can leave long-term footprints within the organism, like in telomeres (TLs), protective chromosome caps that shorten during cell replication and following exposure to stressors. Short TLs are considered to indicate lower fitness prospects, but why TLs shorten under stressful conditions is not understood. In this paper we propose the metabolic telomere attrition hypothesis: during times of substantially increased energy demands, TLs are shortened as part of the transition into an organismal ‘emergency state’, which prioritizes immediate survival functions over processes with longer-term benefits.
Stefania Casagrande and Michaela Hau, "Telomere attrition: Metabolic regulation and signalling function?," Biology Letters 15 (3), 20180885 (2019).
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