We predicted that maternal stress would increase transcription of yolk-processing enzymes and the mitochondrial genes involved in oxidative metabolism. Second, stress influences brain gene expression therefore we predicted that genes associated with neural development might be differentially expressed between embryos of predator-exposed and control mothers. We also predicted that genes involved in eye development might be affected by maternal predator exposure because an earlier study in sticklebacks found that genes associated with eye development were differentially expressed in adults following exposure to predation risk. Third, previous studies have shown that exposing fish embryos to elevated cortisol alters the expression of genes encoding insulinlike growth factor, growth hormone, thyroid hormone receptors, and growth hormone receptors. Since stickleback mothers produce eggs with elevated cortisol after exposure to a predator we predicted that genes that are activated or repressed by cortisol or synthetic glucocorticoids would be differentially expressed between treatments. Three day post-fertilization stickleback embryos do not produce endogenous cortisol. Therefore we did not expect that the key gene products required for HPI axis function, such as corticotropinreleasing hormone, adrenocorticotropic hormone, and proopiomelanocortin to be expressed. Also, since glucocorticoids are known to affect the expression of immunityrelated genes, for example genes of the complement pathway, we predicted an effect of maternal exposure to predation risk on the expression of genes involved in immunity. Fourth, predation pressure is associated with a relatively ‘fast’ life history in many taxa, including sticklebacks therefore we predicted that genes related to accelerated growth and development would be upregulated in embryos as a result of maternal exposure to predation risk. Finally, given the broad epigenetic changes that occur across the genome during tissue differentiation, and previous studies showing that maternal care influences offspring DNA methylation patterns we also predicted that genes involved in epigenetic modifications to the genome, such as the DNA methyltransferases, would be influenced by maternal exposure to predation risk. This unbiased genome-wide expression survey identified some of the molecular mechanisms in embryos that respond to maternal experience. In general, maternal exposure to predation risk had an activating effect on offspring genome-wide expression and affected biological pathways involved in energy homeostasis, proliferation of cells, production of neurites and blood cells, differentiation of sensory neurons, and immunity. Many of these results are consistent with previous findings in sticklebacks and other animals that associated maternal stress with increased offspring growth and metabolism, altered immune function and behavior.