Abstract
In the nematode Caenorhabditis elegans, an insulin receptor signaling pathway regulates adult life span and developmental arrest at the dauer larval stage. Here we show that the unc-64 and unc-31 genes also function in this pathway. These two genes are involved in mediating Ca2+-regulated secretion. Mutations in unc-64 and unc-31 increase adult life span and cause constitutive dauer formation. Both phenotypes are suppressed by mutations in daf-16, which also suppresses other mutations in this pathway. We present evidence that the site of action of unc-64 is neuronal, suggesting that a neurosecretory signal regulates life span and dauer formation.
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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Aging / physiology*
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Animals
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Antigens, Surface / genetics*
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Caenorhabditis elegans / physiology*
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Caenorhabditis elegans Proteins*
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Calcium-Binding Proteins*
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Forkhead Transcription Factors
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Gene Expression Regulation
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Helminth Proteins / genetics*
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Mutation
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Nerve Tissue Proteins / genetics*
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Neurosecretory Systems / physiology*
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Receptor, Insulin / physiology*
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Syntaxin 1
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Transcription Factors / genetics
Substances
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Antigens, Surface
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Caenorhabditis elegans Proteins
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Calcium-Binding Proteins
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Forkhead Transcription Factors
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Helminth Proteins
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Nerve Tissue Proteins
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Syntaxin 1
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Transcription Factors
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UNC-31 protein, C elegans
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daf-16 protein, C elegans
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unc-64 protein, C elegans
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Receptor, Insulin