SOX2 functions to maintain neural progenitor identity

Neuron. 2003 Aug 28;39(5):749-65. doi: 10.1016/s0896-6273(03)00497-5.

Abstract

Neural progenitors of the vertebrate CNS are defined by generic cellular characteristics, including their pseudoepithelial morphology and their ability to divide and differentiate. SOXB1 transcription factors, including the three closely related genes Sox1, Sox2, and Sox3, universally mark neural progenitor and stem cells throughout the vertebrate CNS. We show here that constitutive expression of SOX2 inhibits neuronal differentiation and results in the maintenance of progenitor characteristics. Conversely, inhibition of SOX2 signaling results in the delamination of neural progenitor cells from the ventricular zone and exit from cell cycle, which is associated with a loss of progenitor markers and the onset of early neuronal differentiation markers. The phenotype elicited by inhibition of SOX2 signaling can be rescued by coexpression of SOX1, providing evidence for redundant SOXB1 function in CNS progenitors. Taken together, these data indicate that SOXB1 signaling is both necessary and sufficient to maintain panneural properties of neural progenitor cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cell Cycle / physiology
  • Cell Differentiation / physiology*
  • Central Nervous System / cytology
  • Central Nervous System / embryology*
  • Chick Embryo
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism*
  • Drosophila
  • Gene Expression Regulation, Developmental
  • HMGB Proteins
  • Immunohistochemistry
  • Mice
  • Neurons / physiology*
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism*
  • Phenotype
  • SOXB1 Transcription Factors
  • Signal Transduction / physiology
  • Stem Cells / physiology*
  • Transcription Factors

Substances

  • DNA-Binding Proteins
  • HMGB Proteins
  • Nuclear Proteins
  • SOXB1 Transcription Factors
  • Sox2 protein, mouse
  • Transcription Factors