The SH2/SH3 adaptor protein dock interacts with the Ste20-like kinase misshapen in controlling growth cone motility.
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.
Ruan
W
W
Department of Neurology and Neurosurgery, Centre for Research in Neuroscience, McGill University and The Montreal General Hospital, Québec, Canada.
Pang
P
P
Rao
Y
Y
D048868:Adaptor Proteins, Signal Transducing; D000818:Animals; D001369:Axons / Q000378:metabolism; D002465:Cell Movement / Q000502:physiology; D004330:Drosophila / Q000254:growth & development; D029721:Drosophila Proteins; D005123:Eye / Q000254:growth & development; D020439:Growth Cones / Q000378:metabolism / Q000502:physiology*; D007814:Larva / Q000502:physiology; D008526:Medulla Oblongata / Q000502:physiology; D009154:Mutation / Q000502:physiology; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000502:physiology*; D010641:Phenotype; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*; D014018:Tissue Distribution
D048868:Adaptor Proteins, Signal Transducing; D029721:Drosophila Proteins; D009419:Nerve Tissue Proteins; C099753:dock protein, Drosophila; C113875:msn protein, Drosophila; D017346:Protein Serine-Threonine Kinases