Figure 5.
Mutations in nicotinic acetylcholine receptor subunits suppress ACR-2(L/S)-induced paralysis. A, Quantification of the average number of body bends per minute for wild-type animals, acr-12(ok367), unc-63(ok1075), unc-38(e264), unc-74(e883), and unc-50(e306) mutants in the absence (gray bars) or presence (black bars) of the ACR-2(L/S) transgene. Animals were placed on a food-free agar plate, and the average number of body bends per minute was quantified over a 5 min period. Data represent the mean ± SEM. of at least 10 animals for each genotype. B, Schematic of the membrane topology of ACR-12 with approximate location, allele names, and molecular nature of loss-of-function mutations that suppress ACR-2(L/S) toxicity indicated. C, Quantification of the average number of body bends per minute for the following genotypes: wild type, acr-12(ok367), transgenic ACR-2(L/S), acr-12 mutants expressing ACR-2(L/S), acr-12 mutants expressing ACR-2(L/S) together with an extrachromosomal array containing Punc-47::ACR-12, and acr-12 mutants expressing ACR-2(L/S) together with an extrachromosomal array containing the Pacr-2::ACR-12 cDNA. Data represent the mean ± SEM. for 5–10 animals. D–H, Still images of adult animals on NGM plates without food for the genotypes indicated. “GABA” and “ACh” refer to specific expression of the acr-12 cDNA in GABAergic or cholinergic neurons using the unc-47 or acr-2 promoters, respectively.