[Genetics of early ovarian differentiation: recent data]

Early ovarian development has long been thought of as a default pathway switched on passively by the absence of SRY gene. Recent genetic and transcriptomic studies challenge this view and show that two master pathways simultaneously repress male-specific genes and activate female-specific genetic cascades. This antagonistic action is maintained from embryonic stages to adulthood. The differentiation of the ovarian somatic component is regulated by both the forkhead transcription factor FOXL2 (alone or in combination with oestrogens according to the species) and β-catenin pathway activated by Wnt4 and Rspo1. The sex-specific change in the fate of primordial germ cells depends on the gonad environment. Female gonocytes actively proliferate by mitosis then enter meiosis I until the diplotene stage. Primordial follicle formation occurs when oocytes are individually surrounded with pre-granulosa cells. In mammals, the population of primordial follicles serves as a resting and finite pool of oocytes available during the female reproductive life span. Recent data on factors controlling these molecular processes will be presented in this review.