PUBLICATION

Oligodendrocyte specification in zebrafish requires notch-regulated cyclin-dependent kinase inhibitor function

Authors
Park, H.C., Boyce, J., Shin, J., and Appel, B.
ID
ZDB-PUB-050727-15
Date
2005
Source
The Journal of neuroscience : the official journal of the Society for Neuroscience   25(29): 6836-6844 (Journal)
Registered Authors
Appel, Bruce, Park, Hae-Chul, Shin, Jimann
Keywords
oligodendrocyte; cell cycle; cell fate; neural precursor; neurogenesis; spinal cord
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Cell Differentiation/physiology
  • Cell Division/physiology
  • Cyclin-Dependent Kinase Inhibitor p57/genetics
  • Cyclin-Dependent Kinase Inhibitor p57/metabolism*
  • Female
  • Gene Expression Regulation, Developmental
  • Homeodomain Proteins/genetics
  • Homeodomain Proteins/metabolism*
  • Male
  • Nerve Tissue Proteins/genetics
  • Nerve Tissue Proteins/metabolism*
  • Neurons/cytology
  • Neurons/physiology
  • Oligodendroglia/cytology*
  • Oligodendroglia/physiology*
  • Receptor, Notch1/genetics
  • Receptor, Notch1/metabolism*
  • Signal Transduction/physiology
  • Spinal Cord/cytology
  • Spinal Cord/embryology
  • Spinal Cord/physiology
  • Zebrafish/embryology*
  • Zebrafish/physiology
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
16033893 Full text @ J. Neurosci.
Abstract
Cyclin-dependent kinase inhibitors (Cdkis) influence both cell-cycle progression and differentiation of neural cells. However, the precise roles of Cdkis in coordinating formation of neurons and glia and the mechanisms that regulate expression of genes that encode Cdkis in the vertebrate CNS remain unknown. Here, we report that, in zebrafish, expression of the Cdki gene cyclin-dependent kinase inhibitor 1c (cdkn1c), a p57 homolog, is negatively regulated by Delta-Notch signaling and that Cdkn1c function is required for neural plate cells to stop dividing and differentiate as neurons on schedule, even in the absence of Notch signaling activity. Furthermore, Cdkn1c function is required for specification of oligodendrocytes from ventral spinal cord precursors. We propose that levels of cdkn1c expression are an important factor in regulating neural development: high levels of Cdkn1c promote cell-cycle exit and neuronal development, whereas, during late embryogenesis, neural cells that have low but functional levels of Cdkn1c, regulated by Notch activity, are specified for oligodendrocyte fate.
Genes / Markers
Figures
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Errata and Notes