title: The role of the transcription factor Rbpj in the development of dorsal root ganglia.
abstract: BACKGROUND
  The dorsal root ganglion (DRG) is composed of well-characterized populations of sensory neurons and glia derived from a common pool of neural crest stem cells (NCCs), and is a good system to study the mechanisms of neurogenesis and gliogenesis. Notch signaling is known to play important roles in DRG development, but the full scope of Notch functions in mammalian DRG development remains poorly understood.
  
  
  RESULTS
  In the present study, we used Wnt1-Cre to conditionally inactivate the transcription factor Rbpj, a critical integrator of activation signals from all Notch receptors, in NCCs and their derived cells. Deletion of Rbpj caused the up-regulation of NeuroD1 and precocious neurogenesis in DRG early development but led to an eventual deficit of sensory neurons at later stages, due to reduced cell proliferation and abnormal cell death. In addition, gliogenesis was delayed initially, but a near-complete loss of glia was observed finally in Rbpj-deficient DRG. Furthermore, we found P75 and Sox10, which are normally expressed exclusively in neuronal and glial progenitors of the DRG after the NCCs have completed their migration, were co-expressed in many cells of the DRG of Rbpj conditional knock-out mice.
  
  
  CONCLUSIONS
  Our data indicate that Rbpj-mediated canonical Notch signaling inhibits DRG neuronal differentiation, possibly by regulating NeuroD1 expression, and is required for DRG gliogenesis in vivo.
authors.affiliation: Department of Anatomy and Neurobiology, Tongji University School of Medicine, Shanghai, China. huzelan@hotmail.com
authors.forename: Ze-Lan
authors.initials: ZL
authors.lastname: Hu
authors.forename: Ming
authors.initials: M
authors.lastname: Shi
authors.forename: Ying
authors.initials: Y
authors.lastname: Huang
authors.forename: Min-Hua
authors.initials: MH
authors.lastname: Zheng
authors.forename: Zhe
authors.initials: Z
authors.lastname: Pei
authors.forename: Jia-Yin
authors.initials: JY
authors.lastname: Chen
authors.forename: Hua
authors.initials: H
authors.lastname: Han
authors.forename: Yu-Qiang
authors.initials: YQ
authors.lastname: Ding
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D016923:Cell Death / Q000235:genetics; D002465:Cell Movement / Q000235:genetics; D049109:Cell Proliferation; D004622:Embryo, Mammalian; D005727:Ganglia, Spinal / Q000166:cytology / Q000196:embryology / Q000254:growth & development; D051819:Immunoglobulin J Recombination Signal Sequence-Binding Protein / Q000172:deficiency / Q000378:metabolism*; D051379:Mice; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism; D058953:Neural Stem Cells / Q000502:physiology; D020812:Receptor, trkC / Q000378:metabolism; D011984:Sensory Receptor Cells / Q000502:physiology*; D015854:Up-Regulation / Q000235:genetics; D051155:Wnt1 Protein / Q000235:genetics
chemical_list: D051819:Immunoglobulin J Recombination Signal Sequence-Binding Protein; D009419:Nerve Tissue Proteins; C497571:Rbpj protein, mouse; D051155:Wnt1 Protein; C495246:Wnt1 protein, mouse; D020812:Receptor, trkC