ZFIN ID: ZDB-PUB-030707-12
Delta-Notch signaling regulates oligodendrocyte specification
Park, H.-C. and Appel, B.
Date: 2003
Source: Development (Cambridge, England)   130(16): 3747-3755 (Journal)
Registered Authors: Appel, Bruce, Park, Hae-Chul
Keywords: Delta, Notch, Oligodendrocytes, Motoneurons, Neural precursors, CNS, Spinal cord, Zebrafish
MeSH Terms:
  • Animals
  • Animals, Genetically Modified
  • Basic Helix-Loop-Helix Transcription Factors
  • Cell Differentiation/physiology
  • Cell Lineage
  • Helix-Loop-Helix Motifs
  • Homeodomain Proteins/genetics
  • Homeodomain Proteins/metabolism
  • Hot Temperature
  • Intracellular Signaling Peptides and Proteins
  • Membrane Proteins/genetics
  • Membrane Proteins/metabolism*
  • Nerve Tissue Proteins/genetics
  • Nerve Tissue Proteins/metabolism
  • Neurons/physiology
  • Oligodendroglia/physiology*
  • Receptors, Notch
  • Signal Transduction/physiology*
  • Spinal Cord/cytology
  • Spinal Cord/metabolism
  • Trans-Activators/genetics
  • Trans-Activators/metabolism*
  • Transcription Factors/genetics
  • Transcription Factors/metabolism
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed: 12835391 Full text @ Development
Oligodendrocytes, the myelinating cell type of the central nervous system, arise from a ventral population of precursors that also produces motoneurons. Although the mechanisms that specify motoneuron development are well described, the mechanisms that generate oligodendrocytes from the same precursor population are largely unknown. By analysing mutant zebrafish embryos, we found that Delta-Notch signaling is required for spinal cord oligodendrocyte specification. Using a transgenic, conditional expression system, we also learned that constitutive Notch activity could promote formation of excess oligodendrocyte progenitor cells (OPCs). However, excess OPCs are induced only in ventral spinal cord at the time that OPCs normally develop. Our data provide evidence that Notch signaling maintains subsets of ventral spinal cord precursors during neuronal birth and, acting with other temporally and spatially restricted factors, specifies them for oligodendrocyte fate.