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Genetics, Vol. 167, 633-643, June 2004, Copyright © 2004
doi:10.1534/genetics.103.020230
The GAR-3 Muscarinic Receptor Cooperates With Calcium Signals to Regulate Muscle Contraction in the Caenorhabditis elegans Pharynx
Katherine A. Steger and Leon Avery1
Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9148
1 Corresponding author: Avery Lab, UTSW Medical Center, 6000 Harry Hines Blvd., Room NA5.300, Dallas, TX 75390-9148.
E-mail: leon{at}eatworms.swmed.edu
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 ß-subunit involved in RGS-mediated inhibition of Go
- and Gq-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-dependent processes in the C. elegans pharyngeal muscle.
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