Involvement of Notch-1 in mammalian retinal neurogenesis: association of Notch-1 activity with both immature and terminally differentiated cells

Mech Dev. 1995 Sep;53(1):73-85. doi: 10.1016/0925-4773(95)00425-4.

Abstract

The Notch pathway is thought to define an evolutionarily conserved signaling mechanism that regulates the differentiation of immature cells through cells interactions. We have examined the expression of the Notch-1 receptor, the central element of this pathway, in the developing rat retina, where cell-fate choices depend upon a series of local cell interactions. Notch-1 immunoreactivity is associated with differentiating cells at different stages of retinal neurogenesis, suggesting that Notch-1 may play a role in the successive cell-fate determination which governs retinal development. In addition, the Notch-1 immunoreactivity is detected in nuclei of postmitotic, differentiated neurons of the adult retina. Our observations raise the possibility that besides its role in the differentiation of immature cell populations Notch-1 activity may also be involved in the maintenance of the differentiated state.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Antibodies, Monoclonal
  • Base Sequence
  • Cell Differentiation / physiology
  • Cellular Senescence / physiology
  • Conserved Sequence*
  • Cross Reactions
  • Humans
  • Membrane Proteins / analysis
  • Membrane Proteins / biosynthesis*
  • Membrane Proteins / immunology
  • Middle Aged
  • Mitosis / physiology
  • Molecular Sequence Data
  • Morphogenesis
  • Nerve Tissue Proteins / analysis
  • Nerve Tissue Proteins / biosynthesis*
  • Nervous System / cytology
  • Nervous System / embryology*
  • Neurons / metabolism
  • Rats
  • Receptor, Notch1
  • Receptors, Cell Surface*
  • Retina / embryology*
  • Subcellular Fractions / chemistry
  • Transcription Factors*

Substances

  • Antibodies, Monoclonal
  • Membrane Proteins
  • NOTCH1 protein, human
  • Nerve Tissue Proteins
  • Notch1 protein, rat
  • Receptor, Notch1
  • Receptors, Cell Surface
  • Transcription Factors