Joint maternal and paternal stress increases the cortisol in their daughters' eggs

Background: Parental experience with predators can modify survival- and reproductionrelated traits of offspring via parental effects. Direct predation risk elevates glucocorticoid concentration in the eggs of females, and so indirect predation risk communicated via parental effects may also affect glucocorticoids in the eggs of daughters. Parents may also change their care patterns under predation risk, which could influence the development of the hypothalamus–pituitary–adrenal axis (stress axis) of offspring, which is responsible for the secretion of glucocorticoids. Therefore, in systems where males make substantial contributions to offspring care, paternal effects may also affect daughters' egg glucocorticoids. Question: Are there predator-induced parental effects (maternal, paternal, or joint parental effects) on the concentration of glucocorticoids in daughters' eggs? Organism: Threespine stickleback (Gasterosteus aculeatus) from the Chehalis River, Washington, USA. Freshwater and riverine ecotypes. Methods: We exposed threespine stickleback mothers, fathers, both, or neither to a model predator at developmentally appropriate times using a fully factorial design. Control parents experienced no disturbance. Mothers were exposed to a model predator during egg production and fathers were exposed pre-fertilization and during egg care (but before embryos developed eyes). We then tested the concentration of glucocorticoids in the eggs of daughters using an enzyme-linked immunosorbent assay (ELISA). Results: Daughters of predator-exposed parents (both parents exposed to model predator) had higher glucocorticoid concentrations in their eggs than daughters of control, unexposed parents. Daughters of predator-exposed mothers-only and predator-exposed fathers-only did not differ from controls or jointly predator-exposed parents. Therefore, predator-induced maternal and paternal effects may cumulatively impact the gametes of their daughters, suggesting a mechanism through which predation risk may indirectly influence the next generation (grand-offspring).