Wild and captive vertebrates face multiple stressors that all have the potential to induce chronic maternal stress (i.e., sustained, elevated plasma glucocorticoids), resulting in embryo exposure to elevated maternally derived glucocorticoids. In oviparous taxa such as fish, maternally derived glucocorticoids in eggs are known for their capacity to shape offspring phenotype. Using a variety of methodologies, scientists have quantified maternally derived levels of egg cortisol, the primary glucocorticoid in fishes, and examined the cascading effects of egg cortisol on progeny phenotype. Here we summarize and interpret the current state of knowledge on egg cortisol in fishes and the relationships linking maternal stress/state to egg cortisol and offspring phenotype/fitness. Considerable variation in levels of egg cortisol exists across species and among females within a species; this variation is hypothesized to be due to interspecific differences in reproductive life history and intraspecific differences in female condition. Outcomes of experimental studies manipulating egg cortisol vary both inter- and intraspecifically. Moreover, while exogenous elevation of egg cortisol (as a proxy for maternal stress) induces phenotypic changes commonly considered to be maladaptive (e.g., smaller offspring size), emerging work in other taxa suggests that there can be positive effects on fitness when the offspring's environment is taken into account. Investigations into (i) mechanisms by which egg cortisol elicits phenotypic change in offspring (e.g., epigenetics), (ii) maternal and offspring buffering capacity of cortisol, and (iii) factors driving natural variation in egg cortisol and how this variation affects offspring phenotype and fitness are all germane to discussions on egg glucocorticoids as signals of maternal stress.
Keywords: cortisol; intergenerational effects; match/mismatch; maternal stress; oocyte; phenotype.