Telomere dynamics from hatching to sexual maturity and maternal effects in the “multivariate egg”

Abstract

Avian eggs contain a large number of molecules deposited by the mother that provide the embryo with energy but also potentially influence its development via the effects of maternally-derived hormones and antibodies: the avian egg is “multivariate”. Multivariate effects on offspring phenotype were evaluated in a sister study on captive zebra finches, by simultaneously manipulating maternally derived antibodies after LPS-treatment of mothers and egg-treatment using yolk testosterone injection. LPS-treatment had a positive effect on body mass growth at 30 days after hatching and immune response at sexual maturity, while egg-testosterone positively influenced immune response at fledging and courtship behaviour in sexually mature male offspring. Maternal effects are known to modulate offspring telomere length. Still, the multivariate effects of egg-derived maternal components on offspring telomere dynamics from hatching to sexual maturity are undefined. Here, using the data of the sister study completed with telomere measurements, we tested a) the effects of LPS and T treatments on telomere length (TL) from hatching to sexual maturity (day 82), b) how LPS treatment modulated telomere length over reproduction in adult females, and c) the relationship between maternal and offspring TL. We predicted, a) TL would be shorter in LPS fledglings (as a cost of faster growth), and b) TL would be longer in sexually mature adults from T-treated (as a proxy of individual quality). In adult females, there was an overall negative relationship between laying and rearing investments and telomere length, this relationship being weaker in LPS treated females. In chicks, there was an overall negative effect of LPS treatment on telomere length measured at fledging and sexual maturity (day 25 – 82). In addition, at fledging, there was a sex x LPS x T-treatment interaction, suggesting the existence of antagonistic effects of our treatments. Our data partially support the hypothesis of telomeres are proxies of individual quality and that individual differences in telomere length are set-up very early in life.