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We show that three of the eleven genes of the nematodeCaenorhabditis elegans that mediate resistance to the nematocide levamisole and to other cholinergic agonists encode nicotinic acetylcholine receptor (nAChR) subunits.unc-38 encodes an α subunit while lev-1and unc-29 encode non-α subunits. The nematode nAChR subunits show conservation of many mammalian nAChR sequence features, implying an ancient evolutionary origin of nAChR proteins. Expression in Xenopus oocytes of combinations of these subunits that include the unc-38 α subunit results in levamisole-induced currents that are suppressed by the nAChR antagonists mecamylamine, neosurugatoxin, andd-tubocurarine but not α-bungarotoxin. The mutant phenotypes reveal that unc-38 and unc-29subunits are necessary for nAChR function, whereas thelev-1 subunit is not. An UNC-29–GFP fusion shows that UNC-29 is expressed in body and head muscles. Two dominant mutations oflev-1 result in a single amino acid substitution or addition in or near transmembrane domain 2, a region important to ion channel conductance and desensitization. The identification of viable nAChR mutants in C. elegans provides an advantageous system in which receptor expression and synaptic targeting can be manipulated and studied in vivo.

the journal of neuroscience/the journal of neuroscience

Caenorhabditis elegansLevamisole Resistance Geneslev-1,unc-29, andunc-38Encode Functional Nicotinic Acetylcholine Receptor Subunits