Abstract
Previous genetic studies of intersegmental nerve b development have identified several cell-surface proteins required for correct axon guidance to appropriate target muscles. Here we provide evidence that the small GTPase Drac1 also plays a key role in this guidance process. Neuronal expression of the dominant negative mutation Drac1(N17) causes axons to bypass and extend beyond normal synaptic partners. This phenotype is consistently reproduced by pharmacological blockade of actin assembly. Genetic interactions between Drac1(N17) and the receptor-tyrosine phosphatase Dlar suggest that intersegmental nerve b guidance requires the integration of multiple, convergent signals.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Actins / biosynthesis
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Actins / drug effects
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Animals
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Axons / physiology*
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Cell Movement
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Central Nervous System / embryology
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Cytochalasin D / pharmacology
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Drosophila / embryology*
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Drosophila / physiology
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Drosophila Proteins*
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GTP Phosphohydrolases / genetics
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GTP Phosphohydrolases / physiology*
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GTP-Binding Proteins / genetics
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GTP-Binding Proteins / physiology*
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Genes, Dominant
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Motor Neurons / physiology*
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Muscles / innervation
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Mutation
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Nerve Tissue Proteins / genetics
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Nerve Tissue Proteins / physiology
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Neural Pathways / physiology
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Peripheral Nerves / embryology
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Phenotype
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Protein Tyrosine Phosphatases / genetics
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Protein Tyrosine Phosphatases / physiology
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Receptor-Like Protein Tyrosine Phosphatases, Class 4
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Receptors, Cell Surface*
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rac GTP-Binding Proteins*
Substances
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Actins
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Drosophila Proteins
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Nerve Tissue Proteins
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Rac1 protein, Drosophila
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Receptors, Cell Surface
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beat-Ia protein, Drosophila
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Cytochalasin D
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Protein Tyrosine Phosphatases
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Receptor-Like Protein Tyrosine Phosphatases, Class 4
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GTP Phosphohydrolases
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GTP-Binding Proteins
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rac GTP-Binding Proteins