The G1/G0-like Gα 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.
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