Embryonic germ cells display strikingly different fates with regard to mitosis and meiosis, depending on their sex. In female mice, germ cells switch from mitosis to meiosis shortly after reaching the foetal gonad where they generate the lifelong pool of oocytes. However, in males, meiosis and mitosis are actively repressed, and germ cells remain quiescent in the gonad until birth, when they resume mitosis and start generating spermatocytes. Here (p. ), Philippe Djian and colleagues demonstrate that Basonuclin 2, an extremely conserved transcription factor specifically expressed in male germ cells, suppresses meiosis. More surprisingly, they also show that Basonuclin 2 is required for mitosis repression and, later in life, for meiosis progression during spermatogenesis and maintenance of the spermatogonial stem cells that ensure spermatocyte production during life. Furthermore, Basonuclin 2 is necessary for the expression of DNMT3L, a key protein that is involved in spermatogenesis, and for the repression of meiotic genes (Stra8, Msx1 and Msx2) that are normally expressed in female germ cells. These findings, which uncover a new regulator of male gametogenesis, are likely to further our understanding of spermatogenesis in humans.
