It is often assumed that the transfer of maternal glucocorticoids (GCs; e.g., corticosterone or cortisol) to offspring is an inevitable cost associated with adverse or stressful conditions experienced by mothers. However, recent evidence indicates that maternal GCs may adaptively programme particular physiological and molecular pathways during development to enhance offspring fitness. In this context, an important mechanism through which maternal GCs may lastingly affect offspring phenotypic quality and survival is via effects on embryo telomerase activity and so on offspring postnatal telomere length. Here, using a field experimental design for which we manipulated the corticosterone content in yellow-legged gull (Larus michahellis) eggs, we show that embryos from corticosterone-injected eggs not only had a higher telomerase activity but also longer telomeres just after hatching. A complementary analysis further revealed that gull hatchlings with longer telomeres had a higher survival probability during the period when most of the chick mortality occurs. Given the important role that telomere length and its restoring mechanisms have on ageing trajectories and disease risk, our findings provide a new mechanistic link by which mothers may presumably shape offspring life-history trajectories and phenotype.

中文翻译：

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卵皮质酮可刺激端粒酶活性，促进胚胎发育过程中端粒更长

人们通常认为，将母体糖皮质激素 (GCs；例如，皮质酮或皮质醇) 转移给后代是不可避免的成本，与母亲所经历的不利或压力条件相关。然而，最近的证据表明，母体 GCs 可以在发育过程中适应性地编程特定的生理和分子途径，以增强后代的适应性。在这种情况下，母体 GC 可能持久影响后代表型质量和存活的一个重要机制是通过影响胚胎端粒酶活性等后代出生后端粒长度。在这里，我们使用现场实验设计来控制黄腿鸥 ( Larus michahellis)中的皮质酮含量) 卵，我们发现来自注射皮质酮的卵的胚胎不仅具有更高的端粒酶活性，而且刚刚孵化后的端粒也更长。补充分析进一步表明，端粒较长的幼海鸥在大部分雏鸟死亡发生的时期具有较高的存活概率。鉴于端粒长度及其恢复机制对衰老轨迹和疾病风险的重要作用，我们的研究结果提供了一种新的机制联系，母亲可能通过这种联系塑造后代的生活史轨迹和表型。