The GAR-3 muscarinic receptor cooperates with calcium signals to regulate muscle contraction in the Caenorhabditis elegans pharynx

Genetics
Katherine A Steger, Leon Avery

Abstract

Muscarinic acetylcholine receptors regulate the activity of neurons and muscle cells through G-protein-coupled cascades. Here, we identify a pathway through which the GAR-3 muscarinic receptor regulates both membrane potential and excitation-contraction coupling in the Caenorhabditis elegans pharyngeal muscle. GAR-3 signaling is enhanced in worms overexpressing gar-3 or lacking GPB-2, a G-protein beta-subunit involved in RGS-mediated inhibition of G(o)alpha- and G(q)alpha-linked pathways. High levels of signaling through GAR-3 inhibit pharyngeal muscle relaxation and impair feeding--but do not block muscle repolarization--when worms are exposed to arecoline, a muscarinic agonist. Loss of gar-3 function results in shortened action potentials and brief muscle contractions in the pharyngeal terminal bulb. High levels of calcium entry through voltage-gated channels also impair terminal bulb relaxation and sensitize worms to the toxic effects of arecoline. Mutation of gar-3 reverses this sensitivity, suggesting that GAR-3 regulates calcium influx or calcium-dependent processes. Because the effects of GAR-3 signaling on membrane depolarization and muscle contraction can be separated, we conclude that GAR-3 regulates multiple calcium-...Continue Reading

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Citations

Dec 2, 2010·Invertebrate Neuroscience : in·Sarah LuedtkeRobert J Walker
Sep 23, 2011·The Journal of Biological Chemistry·Jeong-Eui LeeYoung-Ki Paik
Mar 23, 2005·BMC Genomics·Rebecca M FoxDavid M Miller
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Oct 28, 2021·ACS Chemical Neuroscience·Balasubramanian Chellammal MuthubharathiKrishnaswamy Balamurugan

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