Abstract

Predation often has consistent effects on prey behavior and morphology, but whether the physiological mechanisms underlying these effects show similarly consistent patterns across different populations remains an open question. In vertebrates, predation risk activates the hypothalamic-pituitary-adrenal (HPA) axis, and there is growing evidence that activation of the maternal HPA axis can have intergenerational consequences via, for example, maternally-derived steroids in eggs. Here, we investigated how predation risk affects a suite of maternally-derived steroids in threespine stickleback eggs across nine Alaskan lakes that vary in whether predatory trout are absent, native, or have been stocked within the last 25 years. Using liquid chromatography coupled with mass spectroscopy (LC-MS/MS), we detected 20 steroids within unfertilized eggs. Factor analysis suggests that steroids covary within and across steroid classes (i.e. glucocorticoids, progestogens, sex steroids), emphasizing the modularity and interconnectedness of the endocrine response. Surprisingly, egg steroid profiles were not significantly associated with predator regime, although they were more variable when predators were absent compared to when predators were present, with either native or stocked trout. Despite being the most abundant steroid, cortisol was not consistently associated with predation regime. Thus, while predators can affect steroids in adults, including mothers, the link between maternal stress and embryonic development is more complex than a simple one-to-one relationship between the population-level predation risk experienced by mothers and the steroids mothers transfer to their eggs.

Highlights

  • Predation often has consistent effects on prey behavior and morphology, but whether the physiological mechanisms underlying these effects show consistent patterns across different populations remains an open question

  • Despite the many studies comparing morphology, behavior, and life history traits among populations that differ in predation risk, less is known about the predictability of changes in physiological mechanisms underlying these phenotypic responses to predation pressure

  • It is important to note that the LC-MS/MS method used here measures the steroids precisely, covariation among steroids is not due to antibody cross reactivity

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Summary

Introduction

Predation often has consistent effects on prey behavior and morphology, but whether the physiological mechanisms underlying these effects show consistent patterns across different populations remains an open question. Despite the many studies comparing morphology, behavior, and life history traits among populations that differ in predation risk, less is known about the predictability of changes in physiological mechanisms underlying these phenotypic responses to predation pressure. Activation of the HPA axis can decrease the production of sex steroids such as progesterone and estradiol by the hypothalamic-pituitary-gonadal (HPG) axis[25,27,28] This link between the HPA and HPG axes creates a situation in which stressors are likely to influence levels of multiple steroids, not just glucocorticoids[29]. Increases in predation risk have the potential to elicit changes in glucocorticoid and sex steroid levels in a female and to alter the levels of these steroids within her eggs and the developmental environment of her offspring

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