Fig. 4. A model of RA regulation during prenatal and postnatal meiosis. (A) Schematic of a 12.5 dpc female urogenital ridge (UGR). The mesonephros produces an RA-synthesizing enzyme (RALDH2). We postulate that retinoic acid (RA) moves from the mesonephros into the adjacent gonad through open mesonephric tubules. Germ cells resident in the female gonad express RA receptors (RARs) and respond to RA by expressing STRA8. (B) Schematic of a 12.5 dpc male UGR. The RA-degrading enzyme CYP26B1 is produced by somatic cells. We postulate that, although all germ cells express RARs and thus can respond to RA, they are not exposed to sufficient amounts of RA to induce STRA8 production. (C) Schematized cross-section of a seminiferous tubule at 10 days post partum (10 dpp). CYP26 enzymes (CYP26A1, CYP26B1 and CYP26C1) are produced by peritubular myoid (PM) cells, which surround and isolate seminiferous tubules from the rest of the body. Within the seminiferous tubules, Sertoli cells produce RALDH enzymes (RALDH1 and RALDH2) and germ cells express RARs. As germ cells enter meiosis they produce STRA8. We postulate that RA, produced locally within the seminiferous tubules, triggers Stra8 expression in germ cells and, hence, triggers entry into meiosis.