The C. elegans egl-36 gene encodes a Shaw-type potassium channel that
regulates egg-laying behavior. Gain of function [egl-36(gf)] and domin
ant negative [egl-36(dn)] mutations in egl-36 cause reciprocal defects
in egg laying. An egl-36::gfp reporter is expressed in the egg-laying
muscles and in a few other tissues. Expression of an egl-36(gf) cDNA
in the egg-laying muscles causes behavioral defects similar to those o
bserved in egl-36(gf) mutants. Gain of function EGL-36 subunits form c
hannels that are active at more negative potentials than wild-type cha
nnels. The egl-36(gf) alleles correspond to missense mutations in an a
mino terminal subunit assembly domain (E138K) and in the S6 transmembr
ane domain (P435S), neither of which were previously implicated in the
voltage dependence of channel activation. Altogether, these results s
uggest that EGL-36 channels regulate the excitability of the egg-layin
g muscles.