Trio mediates netrin-1-induced Rac1 activation in axon outgrowth and guidance

Mol Cell Biol. 2008 Apr;28(7):2314-23. doi: 10.1128/MCB.00998-07. Epub 2008 Jan 22.

Abstract

The chemotropic guidance cue netrin-1 promotes neurite outgrowth through its receptor Deleted in Colorectal Cancer (DCC) via activation of Rac1. The guanine nucleotide exchange factor (GEF) linking netrin-1/DCC to Rac1 activation has not yet been identified. Here, we show that the RhoGEF Trio mediates Rac1 activation in netrin-1 signaling. We found that Trio interacts with the netrin-1 receptor DCC in mouse embryonic brains and that netrin-1-induced Rac1 activation in brain is impaired in the absence of Trio. Trio(-/-) cortical neurons fail to extend neurites in response to netrin-1, while they are able to respond to glutamate. Accordingly, netrin-1-induced commissural axon outgrowth is reduced in Trio(-/-) spinal cord explants, and the guidance of commissural axons toward the floor plate is affected by the absence of Trio. The anterior commissure is absent in Trio-null embryos, and netrin-1/DCC-dependent axonal projections that form the internal capsule and the corpus callosum are defective in the mutants. Taken together, these findings establish Trio as a GEF that mediates netrin-1 signaling in axon outgrowth and guidance through its ability to activate Rac1.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Animals
  • Brain / abnormalities
  • Brain / cytology
  • Brain / embryology
  • COS Cells
  • Cell Line
  • Cells, Cultured / cytology
  • Chlorocebus aethiops
  • DCC Receptor
  • Enzyme Activation
  • Female
  • Growth Cones / physiology*
  • Growth Cones / ultrastructure
  • Guanine Nucleotide Exchange Factors / deficiency
  • Guanine Nucleotide Exchange Factors / genetics
  • Guanine Nucleotide Exchange Factors / physiology*
  • Humans
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Knockout
  • Nerve Growth Factors / physiology*
  • Netrin-1
  • Neuropeptides / physiology*
  • Oncogene Proteins / physiology
  • Phosphoproteins / deficiency
  • Phosphoproteins / genetics
  • Phosphoproteins / physiology*
  • Protein Interaction Mapping
  • Protein Serine-Threonine Kinases / deficiency
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / physiology*
  • Receptors, Cell Surface / physiology*
  • Spinal Cord / cytology
  • Spinal Cord / embryology
  • Tumor Suppressor Proteins / physiology*
  • p21-Activated Kinases / physiology
  • rac GTP-Binding Proteins / physiology*
  • rac1 GTP-Binding Protein

Substances

  • Adaptor Proteins, Signal Transducing
  • DCC Receptor
  • Dcc protein, mouse
  • Guanine Nucleotide Exchange Factors
  • NTN1 protein, human
  • Nck protein
  • Nerve Growth Factors
  • Neuropeptides
  • Ntn1 protein, mouse
  • Oncogene Proteins
  • Phosphoproteins
  • Rac1 protein, mouse
  • Receptors, Cell Surface
  • Trio protein, mouse
  • Tumor Suppressor Proteins
  • Netrin-1
  • Pak1 protein, mouse
  • Protein Serine-Threonine Kinases
  • p21-Activated Kinases
  • rac GTP-Binding Proteins
  • rac1 GTP-Binding Protein