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* Department of Biomedical Sciences and
Department of Genetics, Development, and Cell Biology, Iowa State University, Ames, Iowa, USA
1Correspondence: Department of Biomedical Sciences, Iowa State University, Ames, IA 50011, USA. E-mail: rjmartin{at}iastate.edu
Sydney Brenner promoted Caenorhabditis elegans as a model organism, and subsequent investigations pursued resistance to the nicotinic anthelmintic drug levamisole in C. elegans at a genetic level. These studies have advanced our understanding of genes associated with neuromuscular transmission and resistance to the antinematodal drug. In lev-8 and lev-1 mutant C. elegans, levamisole resistance is associated with reductions in levamisole-activated whole muscle cell currents. Although lev-8 and lev-1 are known to code for nicotinic acetylcholine receptor (nAChR) subunits, an explanation for why these currents get smaller is not available. In wild-type adults, nAChRs aggregate at neuromuscular junctions and are not accessible for single-channel recording. Here we describe a use of LEV-10 knockouts, in which aggregation is lost, to make in situ recordings of nAChR channel currents. Our observations provide an explanation for levamisole resistance produced by LEV-8 and LEV-1 mutants at the single-channel level.—Qian, H., Robertson, A. P., Powell-Coffman, J. A., and Martin, R. J. Levamisole resistance resolved at the single-channel level in Caenorhabditis elegans.
Key Words: resistance LEV-10 LEV-8 LEV-1 nAChR
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