Further, embryos of predator-exposed mothers were larger, either because they began with more resources or grew more quickly during early development. Many of the physiological systems involved in the embryonic response to maternal exposure to predation risk are evolutionarily conserved between sticklebacks and mammals, amphibians, reptiles and birds. Therefore our results identify molecular mechanisms in offspring that might be altered by maternal experience in other organisms. We detected a significant effect of maternal exposure to predation risk on several genes involved in metabolic processes, including upregulation of genes involved in the delivery of oxygen to tissues, the production of ATP, anaerobic metabolism, and the metabolism of amino acids and lipids. Coupled with the upregulation of many genes involved in the increased proliferation of cells and a previous finding that maternally-stressed stickleback embryos are larger and consume more oxygen, these findings suggest that maternal experience with predators accelerates offspring growth. Maternal exposure to predation risk upregulated several genes involved in the growth, survival, and death of neurites, the differentiating axons and dendrites that newly-forming neurons use to contact one another in offspring. These include genes involved in synapse formation in cortical neurons, the balance between neuronal survival and death during inflammation, and the development of sensory organs, forebrain, mid-brain and pituitary gland. Together these results suggest that exposing a mother to predation risk accelerates the proliferation and differentiation of neurons in her developing embryos. Early changes in the development of the brain and eyes could be a mechanism by which maternal exposure to predation risk influences offspring learning and behavior in sticklebacks. Genes involved in the formation and use of the eye were upregulated, including genes involved in formation of the lens and neurites, differentiation of fiber cells in the lens, and phosphorylation of rhodopsin in the retina. Sanogo et al. measured gene expression changes in the brains of adult sticklebacks exposed to predator cues and found differential regulation of several genes involved in photoreception and phototransduction. Our results suggest that, at the molecular level, the developing embryo visual system might respond in a similar way to indirect exposure to predation risk that the adult visual system does to direct exposure to predation risk. We did not detect a difference in eye diameter between embryos of maternally-stressed and control mothers, possibly due to limitations in our method of measurement, limited statistical power to detect a subtle difference, or a true lack of difference between the embryos. Future studies wishing to understand the influence of maternal stress on the developing embryo visual system might in the developmental program.