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Defects in sensory nerve numbers and growth in mutant Kit and Steel mice

  • Sandra Lourenssen
  • , Benny Motro
  • , Alan Bernstein
  • , Jack Diamond
  • McMaster University
  • Queen's University Kingston
  • University of Toronto

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

The roles in the nervous system of the receptor tyrosine kinase Kit and its ligand, Steel factor, are unclear. We have now found first, that sensory nerve populations are reduced in mutant Kit and Steel mice, implicating Steel-Kit interactions in neuronal development. Second, sensory axonal regeneration (which occurs independently of nerve growth factor, or NGF) is impaired, while collateral sprouting (NGF dependent) is normal. Therefore, there is a selective involvement of Kit signal transduction pathways in nerve growth; supporting this, in wild-type animals Kit was up-regulated in regenerating, but unchanged in sprouting, sensory neurons. The receptor tyrosine kinase Kit thus contrasts with the receptor tyrosine kinase trkA, which is activated by the sprouting stimulus (NGF) but not by the axonal regeneration signal. (C) 2000 Lippincott Williams and Wilkins.

Original languageEnglish
Pages (from-to)1159-1165
Number of pages7
JournalNeuroReport
Volume11
Issue number6
DOIs
StatePublished - 27 Apr 2000

Keywords

  • Axonal regeneration
  • Collateral sprouting
  • DRG neurons
  • NGF
  • Neuron survival
  • Steel factor
  • Stem cell factor
  • Tyrosine kinase
  • c-Kit

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