Physiological Notch signaling promotes gliogenesis in the developing peripheral and central nervous systems

Merritt K. Taylor, Kelly Yeager, Sean J. Morrison

Research output: Contribution to journalArticlepeer-review

145 Scopus citations


Constitutive activation of the Notch pathway can promote gliogenesis by peripheral (PNS) and central (CNS) nervous system progenitors. This raises the question of whether physiological Notch signaling regulates gliogenesis in vivo. To test this, we conditionally deleted Rbpsuh (Rbpj) from mouse PNS or CNS progenitors using Wnt1-Cre or Nestin-Cre. Rbpsuh encodes a DNA-binding protein (RBP/J) that is required for canonical signaling by all Notch receptors. In most regions of the developing PNS and spinal cord, Rbpsuh deletion caused only mild defects in neurogenesis, but severe defects in gliogenesis. These resulted from defects in glial specification or differentiation, not premature depletion of neural progenitors, because we were able to culture undifferentiated progenitors from the PNS and spinal cord despite their failure to form glia in vivo. In spinal cord progenitors, Rbpsuh was required to maintain Sox9 expression during gliogenesis, demonstrating that Notch signaling promotes the expression of a glial-specification gene. These results demonstrate that physiological Notch signaling is required for gliogenesis in vivo, independent of the role of Notch in the maintenance of undifferentiated neural progenitors.

Original languageEnglish (US)
Pages (from-to)2435-2447
Number of pages13
Issue number13
StatePublished - Jul 2007


  • Central nervous system
  • Gliogenesis
  • Mouse
  • Neural crest
  • Neural stem cells
  • Notch
  • Spinal cord

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology


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