
pmid: 12467587
Misshapen (Msn) has been proposed to shut down Drosophila photoreceptor (R cell) growth cone motility in response to targeting signals linked by the SH2/SH3 adaptor protein Dock. Here, we show that Bifocal (Bif), a putative cytoskeletal regulator, is a component of the Msn pathway for regulating R cell growth cone targeting. bif displays strong genetic interaction with msn. Phenotypic analysis indicates a specific role for Bif to terminate R1-R6 growth cones. Biochemical studies show that Msn associates directly with Bif and phosphorylates Bif in vitro. Cell culture studies demonstrate that Msn interacts with Bif to regulate F-actin structure and filopodium formation. We propose that Bif functions downstream of Msn to reorganize actin cytoskeleton in decelerating R cell growth cone motility at the target region.
Neuroscience(all), Recombinant Fusion Proteins, Green Fluorescent Proteins, Growth Cones, Gene Dosage, Protein Serine-Threonine Kinases, Cytoskeletal Proteins, Luminescent Proteins, Drosophila melanogaster, Cell Movement, Animals, Drosophila Proteins, Photoreceptor Cells, Invertebrate, Pseudopodia, Phosphorylation, Eye Proteins, Cells, Cultured, Cytoskeleton, Protein Binding, Signal Transduction
Neuroscience(all), Recombinant Fusion Proteins, Green Fluorescent Proteins, Growth Cones, Gene Dosage, Protein Serine-Threonine Kinases, Cytoskeletal Proteins, Luminescent Proteins, Drosophila melanogaster, Cell Movement, Animals, Drosophila Proteins, Photoreceptor Cells, Invertebrate, Pseudopodia, Phosphorylation, Eye Proteins, Cells, Cultured, Cytoskeleton, Protein Binding, Signal Transduction
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