First published online June 11, 2007
Development 134, 1303e (2007)
© The Company of Biologists Limited
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.
Related articles in Development:
- Physiological Notch signaling promotes gliogenesis in the developing peripheral and central nervous systems
- Merritt K. Taylor, Kelly Yeager, and Sean J. Morrison
Development 2007 134: 2435-2447.
[Abstract]
[Full Text]
