Telomeres are chromosome protectors that shorten during cell replication and in stressful conditions. Developing individuals are susceptible to telomere erosion when their growth is fast and resources limited. This is critical because the rate of telomere attrition in early life is linked to health and life span of adults. The metabolic telomere attrition hypothesis (MeTA) suggests that telomere dynamics can respond to biochemical signals conveying information about the organism’s energetic state. Among these signals are glucocorticoids (hormones that promote catabolic processes, potentially impairing costly telomere maintenance) and nucleotides, which activate anabolic pathways though the cellular enzyme target of rapamycin (TOR) preventing telomere attrition. During the energetically demanding growth phase, the regulation of telomeres in response to two contrasting signals—one promoting telomere maintenance and the other inducing attrition—provides an ideal experimental setting to test MeTa. We studied nestlings of a rapidly developing free-living passerine, the great tit (Parus major), that either received glucocorticoids (Cort-chicks), nucleotides (Nuc-chicks), or a combination of both (NucCort-chicks) all compared with controls (Cnt-chicks). Contrary to Cort-chicks, which showed telomere attrition, NucCort-chicks, did not. NucCort-chicks was the only group showing increased gene expression of telo2 (proxy for TOR activation), of mitochondrial enzymes linked to ATP production (atp5f1a-atp5f1b-cox6a1-cox4) and a higher efficiency in aerobically producing ATP. NucCort-chicks had also a higher expression of telomere maintenance genes (trf2) and of enzymatic antioxidant genes (gpx4-sod1). The findings show that nucleotides availability is crucial for preventing telomere erosion during fast growth in stressful environments.

Reproductive phenotypes are shaped by genetic, physiological and environmental variation that an organism experiences during ontogeny. Steroid hormones play an integrative role in this process through both genomic and non-genomic pathways. Differences in steroid hormone metabolism may be rooted in genomic variation. Here we evaluate the influence of supergene variants underlying alternative reproductive tactics on sex steroid metabolism during ontogeny in ruffs (Calidris pugnax). Adult ruff males exhibit three male mating morphs called Independents, Faeders and Satellites, that differ prominently in circulating androgen (testosterone and androstenedione) concentrations. Across morphs and sexes chicks showed similar mean androgen concentrations during ontogenetic development. However, variances in circulating androgens showed the same pattern as corresponding variances previously observed in adults. HSD17B2 had been previously identified as a key gene for mediating differences in androgen levels between morphs as it encodes the enzyme that converts testosterone to androstenedione and is located within the supergene. Observed HSD17B2 expression in embryonic brain tissue was consistent with predictions based on genetic and endocrine differences. Taken together, the observed differences in circulating androgen concentrations and gene expression point to testosterone synthesis as a key mechanism that shapes developmental trajectories and differences in brain organization among morphs.