Abstract
Sensory signals regulate multiple developmental and behavioral circuits in C. elegans, providing a genetically tractable system in which to investigate the mechanisms underlying the acquisition and integration of sensory information. kin-29 mutants are defective in the expression of a set of chemoreceptor genes, and exhibit characteristics associated with altered sensory signaling, including increased lifespan, decreased body size, and deregulated entry into the dauer developmental stage. kin-29 encodes a Ser/Thr kinase with similarity to the MARK and AMPK/SNF1 family of kinases. We show that KIN-29 acts cell-autonomously and non-cell-autonomously in sensory neurons to regulate chemoreceptor expression, body size, and the dauer decision, suggesting that kin-29 function is essential for the correct acquisition and transduction of sensory information.
MeSH terms
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Active Transport, Cell Nucleus / physiology
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Amino Acid Sequence
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Animals
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Animals, Genetically Modified
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Caenorhabditis elegans / physiology*
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Caenorhabditis elegans Proteins
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Chemoreceptor Cells / physiology*
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Cloning, Molecular
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Gene Expression Regulation*
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Genes, Reporter
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Helminth Proteins / genetics
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Helminth Proteins / metabolism
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Hot Temperature / adverse effects
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Humans
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Life Expectancy
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Molecular Sequence Data
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Mutation
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Neurons, Afferent / physiology*
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Pheromones / metabolism
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Phylogeny
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Protein Serine-Threonine Kinases / chemistry
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Protein Serine-Threonine Kinases / classification
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Protein Serine-Threonine Kinases / genetics
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Protein Serine-Threonine Kinases / metabolism*
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Recombinant Fusion Proteins / genetics
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Recombinant Fusion Proteins / metabolism
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Sequence Alignment
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Signal Transduction*
Substances
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Caenorhabditis elegans Proteins
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Helminth Proteins
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Pheromones
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Recombinant Fusion Proteins
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kin-29 protein, C elegans
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Protein Serine-Threonine Kinases