UNC5A promotes neuronal apoptosis during spinal cord development independent of netrin-1

Nat Neurosci. 2006 Aug;9(8):996-8. doi: 10.1038/nn1736. Epub 2006 Jul 9.


In addition to their role as chemorepellent netrin-1 receptors, UNC5 proteins may mediate cell death because they induce apoptosis in cultured cells. To test this in vivo, we generated Unc5a (formerly Unc5h1) knockout mice and found that this deletion decreased apoptosis and increased the number of neurons in the spinal cord. In contrast, loss of netrin-1 (Ntn1) did not affect the amount of apoptosis, suggesting that NTN1 is not required for neuronal apoptosis in vivo.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / physiology*
  • Mice
  • Mice, Knockout
  • Nerve Growth Factors / genetics
  • Nerve Growth Factors / metabolism*
  • Netrin Receptors
  • Netrin-1
  • Neurons / metabolism*
  • Neurons / pathology
  • Receptors, Cell Surface / genetics
  • Receptors, Cell Surface / metabolism*
  • Spinal Cord / abnormalities
  • Spinal Cord / cytology*
  • Spinal Cord / embryology*
  • Spinal Cord / metabolism
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism*


  • Nerve Growth Factors
  • Netrin Receptors
  • Ntn1 protein, mouse
  • Receptors, Cell Surface
  • Tumor Suppressor Proteins
  • Unc5A protein, mouse
  • Netrin-1