Meeting Abstract
Exposure to elevated glucocorticoids during development can have long-term “programming” effects on phenotype, which are expected to be mediated by changes in gene expression. We tested the hypothesis that transient elevation of corticosterone in semi-precocial seabird chicks (Black-legged kittiwakes (Rissa tridactyla)) induces short-term changes in physiology and behavior, but longer-term effects on gene expression. From day 10 to day 16 post-hatch, free-living chicks from supplementally fed nests were fed (3x/day) with oil containing corticosterone (CORT) or oil only, or were non-handled controls (NHC). We measured baseline corticosterone levels, growth, and behavior. On day 25, we took pectoralis muscle biopsies, then generated a de novo transcriptome assembly and quantified gene expression. Oral corticosterone induced a short-term (detected 15 min but not 60 min after administration) elevation of baseline corticosterone, and did not affect corticosterone secretion post-treatment, development, or begging behavior of chicks. However, 9 days after treatments ended, chicks exhibited differential gene expression across treatments. A significant downregulation of immune-related genes in CORT chicks compared to NHC emerged as the most distinctive pattern (~60% of differentially expressed identified transcripts). Thus despite the apparent ability to tolerate acute elevations in glucocorticoids, young kittiwakes carry an imprint of such exposure that may affect their fitness. Alteration of immune function has long been recognized as a mechanism linking early stress with costs that manifest later in life. Here we identify some of the molecular mechanisms likely to underlie this programming.
