Abstract
Mutations in the unc-17 gene of the nematode Caenorhabditis elegans produce deficits in neuromuscular function. This gene was cloned and complementary DNAs were sequenced. On the basis of sequence similarity to mammalian vesicular transporters of biogenic amines and of localization to synaptic vesicles of cholinergic neurons in C. elegans, unc-17 likely encodes the vesicular transporter of acetylcholine. Mutations that eliminated all unc-17 gene function were lethal, suggesting that the acetylcholine transporter is essential. Molecular analysis of unc-17 mutations will allow the correlation of specific parts of the gene (and the protein) with observed functional defects. The mutants will also be useful for the isolation of extragenic suppressors, which could identify genes encoding proteins that interact with UNC-17.
Publication types
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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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Acetylcholine / metabolism*
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Alleles
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Amino Acid Sequence
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Animals
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Caenorhabditis elegans / chemistry
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Caenorhabditis elegans / cytology
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Caenorhabditis elegans / genetics*
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Caenorhabditis elegans Proteins*
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Carrier Proteins / analysis
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Carrier Proteins / chemistry
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Carrier Proteins / genetics*
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Cloning, Molecular
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Genes, Helminth*
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Helminth Proteins / analysis
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Helminth Proteins / chemistry
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Helminth Proteins / genetics*
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Membrane Transport Proteins*
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Molecular Sequence Data
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Mutation
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Neurons / chemistry*
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Parasympathetic Nervous System / chemistry
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Phenotype
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Sequence Alignment
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Synaptic Vesicles / chemistry*
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Vesicular Acetylcholine Transport Proteins
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Vesicular Transport Proteins*
Substances
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Caenorhabditis elegans Proteins
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Carrier Proteins
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Helminth Proteins
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Membrane Transport Proteins
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Unc-17 protein, C elegans
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Vesicular Acetylcholine Transport Proteins
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Vesicular Transport Proteins
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Acetylcholine