The environmental conditions encountered during an individual’s developmental phase are now recognized as critical determinants of subsequent adult phenotype. Accumulating evidence suggests that the footprint of a challenging development 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 the exposition to stressful events exert on telomeres at different ontogenetic stages in both humans and animals. Within this project I am investigating the physiological routes by which different types of environmental and social stressors determine telomere dynamics and the resulting fitness consequences. I am addressing this goal by relating mitochondrial function and the expression of key genes linking mitochondrial metabolism, to telomere dynamics in wild birds having different life-history traits (i.e. songbirds, cormorants, shearwaters and penguins) and living in different environments (e.g. different environmental temperatures and hemispheres). Another level of investigation is understanding how different telomere phenotypes are related to fitness-related traits (e.g. parental care, reproductive success, physical endurance, risky behaviors and longevity).
This study is about telomeres, which are chromosome protection devices that shorten during cell division under stress conditions. The rate of telomere attrition in early life is related to adult health and lifespan. The results of this study show that the availability of nucleotides in the diet is crucial to prevent the erosion of telomeres during rapid growth in stressful environments.
Casagrande, S.; Loveland, J. L.; Oefele, M.; Boner, W.; Lupi, S.; Stier, A.; Hau, M.: Dietary nucleotides can prevent glucocorticoid-induced telomere attrition in a fast-growing wild vertebrate. Molecular Ecology 32 (19), pp. 5429 - 5447 (2023)
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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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