Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cell Movement / physiology
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Cells, Cultured
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Cytoskeletal Proteins*
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Cytoskeleton / metabolism
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Drosophila Proteins / genetics
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Drosophila Proteins / metabolism*
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Drosophila melanogaster / cytology
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Drosophila melanogaster / embryology
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Drosophila melanogaster / physiology*
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Eye Proteins / genetics
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Eye Proteins / metabolism*
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Gene Dosage
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Green Fluorescent Proteins
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Growth Cones / metabolism*
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Luminescent Proteins / genetics
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Luminescent Proteins / metabolism
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Phosphorylation
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Photoreceptor Cells, Invertebrate / cytology
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Photoreceptor Cells, Invertebrate / physiology
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Protein Binding
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Protein Serine-Threonine Kinases / genetics
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Protein Serine-Threonine Kinases / metabolism*
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Pseudopodia / metabolism
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Recombinant Fusion Proteins / genetics
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Recombinant Fusion Proteins / metabolism
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Signal Transduction / physiology*
Substances
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Cytoskeletal Proteins
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Drosophila Proteins
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Eye Proteins
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Luminescent Proteins
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Recombinant Fusion Proteins
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bif protein, Drosophila
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Green Fluorescent Proteins
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msn protein, Drosophila
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Protein Serine-Threonine Kinases