Becoming glial in the neural retina

Dev Dyn. 2001 Jun;221(2):146-53. doi: 10.1002/dvdy.1145.


During development of the vertebrate neural retina, multipotent stem cells give rise to retinal neurons as well as to Müller cells, the principal glial population in the retina. Recent studies have shed light upon the extracellular and intracellular signaling pathways that regulate Müller glial cell genesis. Emerging evidence demonstrates that activation of the Notch signaling pathway can play a role in regulating Müller cell development as well as gliogenesis in other parts of the central nervous system. Cyclin dependent kinase (CDK) inhibitors of the Cip/Kip subfamily are cell cycle regulators that can regulate progenitor proliferation during retinal development, but also regulate the proliferation of Müller glia when they become activated in response to stress or injury. Surprisingly this class of proteins can also promote the development of Müller glia. In this review we discuss the role of both Notch and the CDK inhibitors in regulating Müller cell development.

Publication types

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

MeSH terms

  • Animals
  • Cell Cycle
  • Cell Division
  • Cyclin-Dependent Kinases / metabolism
  • Drosophila
  • Drosophila Proteins
  • Gene Expression Regulation, Developmental*
  • Membrane Proteins / metabolism
  • Mice
  • Models, Biological
  • Neuroglia / metabolism*
  • Neurons / physiology*
  • Receptors, Notch
  • Retina / embryology*
  • Signal Transduction
  • Xenopus


  • Drosophila Proteins
  • Membrane Proteins
  • N protein, Drosophila
  • Receptors, Notch
  • Cyclin-Dependent Kinases