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Levamisole resistance resolved at the single‐channel level in Caenorhabditis elegans
Author(s) -
Qian Hai,
Robertson Alan P.,
PowellCoffman Jo Anne,
Martin Richard J.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.08-110502
Subject(s) - caenorhabditis elegans , nicotinic acetylcholine receptor , levamisole , biology , nicotinic agonist , mutant , acetylcholine receptor , ion channel , microbiology and biotechnology , pharmacology , gene , genetics , receptor , immunology
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. FASEB J. 22, 3247–3254 (2008)