The SH2/SH3 adaptor protein dock interacts with the Ste20-like kinase misshapen in controlling growth cone motility

Neuron. 1999 Nov;24(3):595-605. doi: 10.1016/s0896-6273(00)81115-0.


Recent studies suggest that the SH2/SH3 adaptor Dock/Nck transduces tyrosine phosphorylation signals to the actin cytoskeleton in regulating growth cone motility. The signaling cascade linking the action of Dock/Nck to the reorganization of cytoskeleton is poorly understood. We now demonstrate that Dock interacts with the Ste20-like kinase Misshapen (Msn) in the Drosophila photoreceptor (R cell) growth cones. Loss of msn causes a failure of growth cones to stop at the target, a phenotype similar to loss of dock, whereas overexpression of msn induces pretarget growth cone termination. Physical and genetic interactions between Msn and Dock indicate a role for Msn in the Dock signaling pathway. We propose that Msn functions as a key controller of growth cone cytoskeleton in response to Dock-mediated signals.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Animals
  • Axons / metabolism
  • Cell Movement / physiology
  • Drosophila / growth & development
  • Drosophila Proteins*
  • Eye / growth & development
  • Growth Cones / metabolism
  • Growth Cones / physiology*
  • Larva / physiology
  • Medulla Oblongata / physiology
  • Mutation / physiology
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / physiology*
  • Phenotype
  • Protein-Serine-Threonine Kinases / genetics
  • Protein-Serine-Threonine Kinases / metabolism*
  • Tissue Distribution


  • Adaptor Proteins, Signal Transducing
  • Drosophila Proteins
  • Nerve Tissue Proteins
  • dock protein, Drosophila
  • msn protein, Drosophila
  • Protein-Serine-Threonine Kinases