Hormonally mediated maternal effects shape offspring survival potential in stressful environments.
In most egg-laying vertebrates, maternal responses to stressful conditions are translated into the release of glucocorticoid hormones such as cortisol, which are then transmitted to their developing embryos. Although such maternally transmitted hormonal resources have been shown to influence or even interfere with the optimal developmental trajectories of offspring in many taxa, their influence on the dynamics of wild fish populations remains largely unexplored. Here, we examined the extent to which simulated hormonally mediated maternal effects influence the development and early survival of the coral reef damselfish, Pomacentrus amboinensis. Concentrations of cortisol in the eggs were manipulated within naturally occurring limits by immersion. We found that the proportion of embryos that delayed hatching when exposed to high levels of cortisol was considerably lower than in the other two treatments (low cortisol dose and control). High cortisol levels in P. amboinensis eggs resulted in increased egg mortality and greater asymmetry in hatchlings. For embryos that successfully hatched, individuals from the elevated cortisol treatments (especially low dose) survived longer after hatching. Although individuals that originated from eggs with elevated cortisol levels survived longer after hatching, they may not gain an overall survival advantage. Our results suggest that subtle increases in the allocation of maternally derived hormones, such as cortisol, to offspring are a direct way for stressed mothers to endow their young with an immediate survival advantage. We propose that this immediate benefit outweighs the developmental costs which may be expressed as reduced fitness at later life stages.
Gagliano
Monica
M
School of Marine and Tropical Biology, James Cook University, Townsville, QLD, Australia. monica.gagliano@jcu.edu.au
McCormick
Mark I
MI
D000704:Analysis of Variance; D000818:Animals; D004625:Embryo, Nonmammalian / Q000187:drug effects / Q000196:embryology; D006854:Hydrocortisone / Q000378:metabolism* / Q000494:pharmacology; D010063:Ovum / Q000187:drug effects / Q000378:metabolism; D010473:Perciformes / Q000378:metabolism*; D010641:Phenotype; D016019:Survival Analysis
D006854:Hydrocortisone