TY - JOUR
T1 - The Gα protein ODR-3 mediates olfactory and nociceptive function and controls cilium morphogenesis in C. elegans olfactory neurons
AU - Roayaie, Kayvan
AU - Crump, Justin Gage
AU - Sagasti, Alvaro
AU - Bargmann, Cornelia I.
N1 - Funding Information:
We are grateful to Orion Weiner and John Sedat for their guidance in deconvolution microscopy. We thank Henry Bourne, Ira Herskowitz, Richard Axel, Sue Kirch, Jen Zallen, and Emily Troemel for discussion and comments on the manuscript; Hernan Espinoza, Andrew Shiau, and Ramon Tabtiang for advice, reagents, and valuable discussions; Jim Thomas for the odr-3(n1605) strain; Simon Tuck and Iva Greenwald for the arP3 strain; Bob Barstead for the cDNA library; Emily Troemel for the STR-2::GFP fusion gene; Andy Fire for the GFP vector; and the Caenorhabditis Genetic Center for some strains used in this work. This work was supported by the Howard Hughes Medical Institute. K. R., J. G. C., and A. S. are Predoctoral Fellows of the Howard Hughes Medical Institute, and C. I. B. is an Assistant Investigator of the Howard Hughes Medical Institute.
PY - 1998/1
Y1 - 1998/1
N2 - 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.
AB - 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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U2 - 10.1016/S0896-6273(00)80434-1
DO - 10.1016/S0896-6273(00)80434-1
M3 - Article
C2 - 9459442
AN - SCOPUS:0031934849
SN - 0896-6273
VL - 20
SP - 55
EP - 67
JO - Neuron
JF - Neuron
IS - 1
ER -