Indicates that it could emerge as a key reporter system in systems and synthetic biology. Non-genetic maternal effects, or the influence of a mother’s phenotype on her offspring phenotype, are widespread across taxa. Mothers can affect offspring phenotype by the level of care they give, and the resources they provide including steroids transferred to developing offspring. Maternal effects can be adaptive, conveying information about the environment that offspring are likely to encounter or maladaptive, and have been associated with human disease. However we know little about the molecular mechanisms by which maternal experience influences offspring. Studies on diverse organisms have shown that maternal stress can have long-lasting effects on offspring traits including survival, growth, morphology, and behavior. While stress-induced maternal effects can be mediated by differential provisioning of resources by mothers, stress-induced maternal effects are often mediated by prenatal exposure to maternally-derived stress hormones. Prenatal exposure to maternally-derived stress hormones can have organizational effects on development with lifelong consequences for offspring. Predators are one of the most important naturally-occurring stressors for animals in natural populations, influencing both evolved and plastic life history traits of prey such as growth, age at reproduction and size at reproduction. A number of recent studies have shown consequences of in utero exposure to predation risk. For example, predator-exposed female sticklebacks produced larger eggs with higher concentrations of cortisol and, initially, a higher metabolism. Later in life, offspring of predator-exposed stickleback mothers exhibited greater antipredator behavior, an altered stress response to predation risk, and performed relatively poorly in a learning task. Maternal exposure to predation risk also influenced offspring survival in sticklebacks. These results are consistent with the hypothesis that maternal exposure to predation risk has organizational effects on the development of the offspring brain and HPI axis that influences offspring traits well into adulthood. Despite growing appreciation of maternal effects occur across taxa and traits, we are just beginning to understand the molecular mechanisms by which maternal experience influences offspring. Therefore, we used RNA-sequencing technology to compare the stickleback embryonic transcriptomes of predator-exposed mothers and unexposed mothers. We measured embryos at three days post-fertilization because in zebrafish it is the earliest period when maternally-derived RNAs are thought to be fully degraded and when brain regions begin to develop. We made the following predictions about the types of genes and pathways likely to be influenced by maternal exposure to predation risk. First, because embryos from maternally-stressed stickleback mothers had higher initial.