Essential to sexual reproduction is the generation of haploid gametes from diploid germ cells through meiosis – a specialised reductive form of cell division that occurs exclusively in the germline. Despite its importance, the molecular mechanisms underlying the transition from mitosis to meiosis remains poorly understood. Germ cells initiate meiosis during fetal life in females and at puberty in males. This temporal difference is widely believed to be dependent solely on the gonadal environment established by the somatic cellular population, not the chromosome constitution of the germ cells (XX vs XY). In females, the extrinsic signalling molecule retinoic acid (RA) activates a meiotic gatekeeper, Stra8, which is indispensable for meiosis in both sexes. Nonetheless, other signalling factors such as bone morphogenetic proteins (BMP) are also likely to be involved to ensure germ cells embark on meiosis at the right time.
Recent work of Miyauchi et al. suggested BMP may be required in addition to RA to induce the female fate in primordial germ cell-like cells in vitro. To investigate whether and how BMP signalling is required in vivo, we assessed a mouse model deficient for BMP receptor 1A and showed that germ cell-specific loss of BMP signalling does not impact on Stra8 expression, but does delay meiotic onset and progression in female fetal germ cells. More experiments are currently underway to identify potential downstream targets of BMP in fetal ovaries, and to thoroughly unveil the molecular mechanisms underlying a timely meiotic transition and efficient progression in mouse germ cells.