Abstract
Axons are defined by the presence of presynaptic specializations at specific locations. We show here that loss-of-function mutations in the C. elegans gene syd-1 cause presynaptic specializations to form in the dendritic processes of GABA-expressing motor neurons during initial differentiation. At a later developmental stage, however, syd-1 is not required for the polarity respecification of a subset of these neurons. The SYD-1 protein contains PDZ, C2 and rho-GTPase activating protein (GAP)-like domains, and is localized to presynaptic terminals in mature neurons. A truncated SYD-1 that lacks the rhoGAP domain interferes with neurite outgrowth and guidance. Our data indicate that syd-1 may be involved in specifying axon identity during initial polarity acquisition.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Axons / chemistry
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Axons / physiology*
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Caenorhabditis elegans
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Caenorhabditis elegans Proteins / chemistry
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Caenorhabditis elegans Proteins / genetics*
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Caenorhabditis elegans Proteins / metabolism*
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GTPase-Activating Proteins / chemistry
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Gene Expression Regulation, Developmental
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Larva
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Molecular Sequence Data
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Mutation, Missense / physiology
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Neurites / chemistry
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Neurites / physiology
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Neurons / physiology
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Presynaptic Terminals / chemistry
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Presynaptic Terminals / physiology*
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Protein Structure, Tertiary
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Sequence Homology, Amino Acid
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Spinal Cord / cytology
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Spinal Cord / embryology
Substances
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Caenorhabditis elegans Proteins
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GTPase-Activating Proteins
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SYD-1 protein, C elegans
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rho GTPase-activating protein