During gonadogenesis in mice, cells within the coelomic endothelium (CE) proliferate to give rise to additional CE cells as well as somatic cells of the gonads. But how is this cell fate decision – CE versus gonadal – determined? In this issue, Blanche Capel and colleagues show that NUMB, a known antagonist of Notch signalling, plays a central role (p. 1607). They show that, during early gonadogenesis in mice, NUMB is asymmetrically localised to the basolateral domain of CE cells, which also exhibit high levels of Notch signalling. Importantly, the authors report that the temporal deletion of Numb results in gonadal defects; mutant gonads contain patches of undifferentiated cells, reduced numbers of differentiated somatic cells and, curiously, reduced numbers of germ cells. The polarity of CE cells in mutant gonads is also disrupted. Finally, the researchers demonstrate that blocking Notch signalling (using the g-secretase inhibitor DAPT) can rescue the somatic cell defects. Based on their findings, the authors propose that asymmetric divisions in the CE give rise to one daughter that remains in the CE, and one daughter that inherits NUMB and the competence to differentiate.
