Abstract
Six mutants of SLO-1, a large-conductance, Ca(2+)-activated K(+) channel of C. elegans, were obtained in a genetic screen for regulators of neurotransmitter release. Mutants were isolated by their ability to suppress lethargy of an unc-64 syntaxin mutant that restricts neurotransmitter release. We measured evoked postsynaptic currents at the neuromuscular junction in both wild-type and mutants and observed that the removal of SLO-1 greatly increased quantal content primarily by increasing duration of release. The selective isolation of slo-1 as the only ion channel mutant derived from a whole genomic screen to detect regulators of neurotransmitter release suggests that SLO-1 plays an important, if not unique, role in regulating neurotransmitter release.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Amino Acid Sequence
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Animals
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Caenorhabditis elegans / genetics
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Caenorhabditis elegans / metabolism
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Caenorhabditis elegans Proteins
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Excitatory Postsynaptic Potentials / physiology
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Large-Conductance Calcium-Activated Potassium Channels
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Molecular Sequence Data
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Mutation / genetics
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Neuromuscular Junction / genetics
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Neuromuscular Junction / metabolism*
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Neurotransmitter Agents / genetics
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Neurotransmitter Agents / metabolism*
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Potassium Channels / physiology*
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Potassium Channels, Calcium-Activated / genetics
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Potassium Channels, Calcium-Activated / metabolism
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Potassium Channels, Calcium-Activated / physiology*
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Presynaptic Terminals / metabolism
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Xenopus
Substances
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Caenorhabditis elegans Proteins
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Large-Conductance Calcium-Activated Potassium Channels
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Neurotransmitter Agents
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Potassium Channels
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Potassium Channels, Calcium-Activated
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slo-1 protein, C elegans
Associated data
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GENBANK/AF431891
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GENBANK/AF431892
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GENBANK/AF431893