Résumé
Stressful conditions experienced during early life are expected to be highly detrimental to fitness. Mechanisms to cope with early-life stress are common in nature, although their molecular basis and fitness consequences remain challenging to study in wild populations. In this study, we use blood transcriptomics, morphological, and life history data to test whether king penguins hatching late in the breeding season experience detrimental effects of a more adverse growth environment. We show that late-born penguins display different gene expression patterns in pathways linked to stress responses, but also in homeostasis maintenance. We detected 35 DEGs related to stress, development, cell growth, and homeostasis. Five over-expressed genes in late-born chicks involved in stress response and homeostasis were also hub genes in a gene co-expression module related with late phenology, supporting our hypothesis that late-born individuals are under higher stress levels. Likely as a consequence of early-life stress and energy allocation to homeostasis regulation, late-born chicks also fledge smaller and with lower body condition, and display under-expression of genes related to proper development (notably RPL22L1, HIBCH, and CALM2). Despite these differences, the return rate of late-borns was not significantly different from early-borns in early adult life, suggesting that, when surviving to fledging, early-life stress was successfully curbed, showing no carryover effects in the first years post-fledging. Overall, our study highlights both the wide-ranging impact of early-life adversity on growth in this wild species, and the importance of resilience mechanisms that compensate for this adversity in early- and late-born king penguins.