rax, Hes1, and notch1 promote the formation of Müller glia by postnatal retinal progenitor cells

Neuron. 2000 May;26(2):383-94. doi: 10.1016/s0896-6273(00)81171-x.


We are interested in the mechanisms of glial cell development in the vertebrate central nervous system. We have identified genes that can direct the formation of glia in the retina. rax, a homeobox gene, Hes1, a basic helix-loop-helix gene, and notch1, a transmembrane receptor gene, are expressed in retinal progenitor cells, downregulated in differentiated neurons, and expressed in Müller glia. Retroviral transduction of any of these genes resulted in expression of glial markers. In contrast, misexpression of a dominant-negative Hes1 gene reduced the number of glia. Cotransfection of rax with reporter constructs containing the Hes1 or notch1 regulatory regions led to the upregulation of reporter transcription. These data suggest a regulatory heirarchy that controls the formation of glia at the expense of neurons.

Publication types

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

MeSH terms

  • 3T3 Cells
  • Animals
  • Animals, Newborn / physiology
  • Basic Helix-Loop-Helix Transcription Factors
  • Biomarkers
  • Cell Differentiation / physiology
  • Cell Division / physiology
  • Eye Proteins / physiology*
  • Gene Expression / physiology
  • Genes, Dominant / physiology
  • Homeodomain Proteins / genetics
  • Homeodomain Proteins / physiology*
  • Membrane Proteins / physiology*
  • Mice
  • Neuroglia / cytology*
  • Rats
  • Receptor, Notch1
  • Receptors, Cell Surface*
  • Retina / cytology*
  • Stem Cells / cytology
  • Transcription Factor HES-1
  • Transcription Factors*
  • Up-Regulation


  • Basic Helix-Loop-Helix Transcription Factors
  • Biomarkers
  • Eye Proteins
  • Hes1 protein, mouse
  • Hes1 protein, rat
  • Homeodomain Proteins
  • Membrane Proteins
  • Notch1 protein, mouse
  • Notch1 protein, rat
  • Rax protein, mouse
  • Receptor, Notch1
  • Receptors, Cell Surface
  • Transcription Factor HES-1
  • Transcription Factors