In mammalian species, the process of meiosis, in which genes are randomly assorted between parental chromosomes during formation of egg and sperm cells, occurs prenatally in females but postnatally in males. To understand sex-specific differences in signaling mechanisms that underlie fertility, many studies have focused on identifying factors that control meiotic induction. Studies in mice using genetic knockout of the transcriptional regulator Polycomb repressive complex–1 (PRC1) and pharmacological inhibition of retinoic acid (RA) signaling suggest that PRC1 prevents female meiotic induction until release of PRC1 repression by increased RA signaling in the ovary. However, genetic studies with mice lacking RA synthesis in reproductive tissues indicate that RA is required for male but not female meiosis, suggesting that RA functions as a male-specific inducer of meiosis and that another factor releases PRC1 repression to initiate female meiosis. Correct resolution of the molecular events governing female and male meiosis is important for treating infertility and devising improved birth control strategies.