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Journal of Neuroscience, Vol 7, 3059-3071, Copyright © 1987 by Society for Neuroscience
Cholinergic receptor mutants of the nematode Caenorhabditis elegans
JA Lewis, JS Elmer, J Skimming, S McLafferty, J Fleming and T McGee
Department of Biological Sciences, University of Missouri, Columbia 65211.
Potential acetylcholine receptor (AChR) mutants of the nematode are
selectable by resistance to the neurotoxic drug levamisole, a probable
cholinergic agonist. To determine which mutants may have achieved
resistance through loss of levamisole receptor function, we have assayed
mutant extracts for specific 3H-meta-aminolevamisole binding activity in
the presence and absence of mecamylamine. We find that mutants in 3 of the
7 genes associated with extreme levamisole resistance are obviously
deficient in saturable specific 3H-meta- aminolevamisole binding activity.
Mutants of the 4 other genes have abnormal binding activities that fail to
undergo the apparent allosteric activation of saturable specific
3H-meta-aminolevamisole binding activity caused by mecamylamine. Thus, all
7 genes appear to be required to produce a fully functional levamisole
receptor. Mutants of several other genes associated only with partial
resistance to levamisole have at least grossly normal receptor binding
activities.
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