Voltage-dependent potassium channels are thought to play an important role in regulating the excitability of cells. Little is known about their contribution to cell excitability in a behaving organism. We present here the behavioral, genetic, molecular, and biophysical analysis of the C. elegans
egl-36 gene which encodes a Shaw-type potassium channel. Dominant and recessive mutations in
egl-36 cause reciprocal egg-laying defects.
egl-36(lf) mutations cause an egg-laying constitutive phenotype, while
egl-36(dm) mutations cause an egg-laying defective phenotype. Consistent with EGL-36 channels regulating egg-laying muscle excitability, the
egl-36 gene is expressed in the egg-laying muscles. In addition, EGL-36 is also expressed in head and defecation muscles, as well as several other neurons and non-neuronal tissues. Expression of wild type EGL-36 channels in tissue culture cells and analysis of whole cell currents revealed a novel non-inactivating delayed rectifier potassium current. Analysis of dominant EGL-36 channel mutants
n728 and
n2332 showed that mutant channels formed by these subunits are active at more negative potentials. These mutations fall in regions S1 and S6, respectively, regions unknown previously to affect the voltage sensitivity of voltage-dependent potassium channels. Thus, dominant EGL-36 mutant channels are inappropriately active and may cause the observed egg-laying defective phenotype by opposing the normal activation of the egg-laying muscles. Taken together these studies show that EGL-36 channels play an important role in regulating the excitability of the egg-laying muscles.