Genes controlling ion permeability in both motorneurons and muscle.

ABSTRACT

Genetic data suggest that unc-8 is a member of the epithelial sodium channel (ENaC) gene family (shreffler et al., 1995). Consistent with this idea, cosmid R13A1, containing an ENaC homolog, can restore normal locomotion to unc-8 mutants after germline transformation. To identify other genes encoding proteins that regulate ENaC function, extragenic unc-8 suppressor and enhancer mutations were sought. This report describes two new unc-8 suppressor mutations, sup-42(lb88) X and sup-43(lb141) II, and an enhancer mutation, enu-2(lb140) III. sup-43(lb141) and enu-2(lb140), cause vacuoles within body wall muscle, similar in appearance to those of unc-105(n490) II mutants, consistent with their proposed role in ENaC function. Single and double mutant phenotypes observed in this and previous work suggest that sodium channels in different tissues utilize an overlapping set of gene products at least six in motorneurons, unc-8, mec-6, and sup-40-43, and at least five in muscle, sup-43, unc-8, enu-2, unc-105, and mec-6.