Abstract
The Gi/Go-like G alpha protein ODR-3 is strongly and selectively implicated in the function of C. elegans olfactory and nociceptive neurons. Either loss of odr-3 function or overexpression of odr-3 causes severe olfactory defects, and odr-3 function is essential in the ASH neurons that sense noxious chemical and mechanical stimuli. In the nociceptive neurons, ODR-3 may interact with OSM-9, a channel similar to the mammalian capsaicin receptor implicated in pain sensation; in AWC olfactory neurons, ODR-3 may interact with another signal transduction pathway. ODR-3 exhibits an unexpected ability to regulate morphogenesis of the olfactory cilia. In odr-3 null mutants, the fan-like AWC cilia take on a filamentous morphology like normal AWA cilia, whereas ODR-3 overexpression in AWA transforms its filamentous cilia into a fan-like morphology.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Sequence
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Animals
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Avoidance Learning / physiology
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Base Sequence
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Caenorhabditis elegans / physiology*
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Caenorhabditis elegans Proteins*
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Cilia / physiology*
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GTP-Binding Protein alpha Subunits, Gi-Go*
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GTP-Binding Proteins / genetics
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GTP-Binding Proteins / metabolism
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GTP-Binding Proteins / physiology*
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Heterotrimeric GTP-Binding Proteins*
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Mechanoreceptors / physiopathology
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Molecular Sequence Data
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Mutation
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Neurons, Afferent / metabolism
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Neurons, Afferent / physiology*
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Nociceptors / physiology*
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Nociceptors / physiopathology
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Olfactory Pathways / cytology
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Olfactory Pathways / physiology*
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Sensation Disorders / genetics
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Sensation Disorders / physiopathology
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Smell / physiology
Substances
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Caenorhabditis elegans Proteins
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odr-3 protein, C elegans
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GTP-Binding Proteins
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GTP-Binding Protein alpha Subunits, Gi-Go
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Heterotrimeric GTP-Binding Proteins