Notching up gliogenesis

Constitutive Notch (N) overexpression promotes gliogenesis, but does this reflect the true physiological role of N signalling? To answer this question,Sean Morrison's group conditionally deleted Rbpsuh - which encodes the DNA-binding protein RBP/J and is required for canonical signalling by all N receptors - in the mouse central (CNS) and peripheral (PNS) nervous systems. Their results on p. 2435 show that N signalling regulates gliogenesis independently of its role in neural progenitor maintenance. The conditional deletion of Rbpsuh in neural crest stem cells and in neuroectodermal cells of the developing CNS causes a near complete loss of gliogenesis, despite neurogenesis occurring almost as normal. These defects, the authors show, are not due to the premature depletion of neural progenitors. Rbpsuh, the authors report, is also required to maintain Sox9 (a glial specification gene) expression in spinal cord progenitors, demonstrating that N signalling acts in glial specification. Together, these findings reveal a reiterative role for N signalling in neurogenesis; initially promoting progenitor maintenance and later promoting gliogenesis.