Rac3-induced neuritogenesis requires binding to Neurabin I

Mol Biol Cell. 2006 May;17(5):2391-400. doi: 10.1091/mbc.e05-08-0753. Epub 2006 Mar 8.

Abstract

Rac3, a neuronal GTP-binding protein of the Rho family, induces neuritogenesis in primary neurons. Using yeast two-hybrid analysis, we show that Neurabin I, the neuronal F-actin binding protein, is a direct Rac3-interacting molecule. Biochemical and light microscopy studies indicate that Neurabin I copartitions and colocalizes with Rac3 at the growth cones of neurites, inducing Neurabin I association to the cytoskeleton. Moreover, Neurabin I antisense oligonucleotides abolish Rac3-induced neuritogenesis, which in turn is rescued by exogenous Neurabin I but not by Neurabin I mutant lacking the Rac3-binding domain. These results show that Neurabin I mediates Rac3-induced neuritogenesis, possibly by anchoring Rac3 to growth cone F-actin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Animals
  • Cells, Cultured
  • Cytoskeleton / chemistry
  • Cytoskeleton / metabolism
  • Growth Cones / chemistry
  • Growth Cones / metabolism
  • Growth Cones / physiology*
  • Immunoprecipitation
  • Mice
  • Microfilament Proteins / analysis
  • Microfilament Proteins / genetics
  • Microfilament Proteins / metabolism*
  • Mutation
  • Nerve Tissue Proteins / analysis
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism*
  • Neurites / chemistry
  • Neurites / physiology*
  • Neurons / cytology
  • Neurons / metabolism
  • Neurons / physiology
  • Nuclear Receptor Coactivator 3
  • Oligodeoxyribonucleotides, Antisense / genetics
  • Oligodeoxyribonucleotides, Antisense / pharmacology
  • Protein Interaction Mapping
  • Protein Structure, Tertiary
  • Rats
  • Transcription Factors / analysis
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • Transcriptional Activation

Substances

  • Actins
  • Microfilament Proteins
  • Nerve Tissue Proteins
  • Oligodeoxyribonucleotides, Antisense
  • Transcription Factors
  • neurabin
  • Nuclear Receptor Coactivator 3

Grants and funding