Behavioral defects in C. elegans egl-36 mutants result from potassium channels shifted in voltage-dependence of activation.
Mutations in the C. elegans egl-36 gene result in defective excitation of egg-laying and enteric muscles. Dominant gain-of-function alleles inhibit enteric and egg-laying muscle contraction, whereas a putative null mutation has no observed phenotype. egl-36 encodes a Shaw-type (Kv3) voltage-dependent potassium channel subunit. In Xenopus oocytes, wild-type egl-36 expresses noninactivating channels with slow activation kinetics. One gain-of-function mutation causes a single amino acid substitution in S6, and the other causes a substitution in the cytoplasmic amino terminal domain. Both mutant alleles produce channels dramatically shifted in their midpoints of activation toward hyperpolarized voltages. An egl-36::gfp fusion is expressed in egg-laying muscles and in a pair of enteric muscle motor neurons. The mutant egl-36 phenotypes can thus be explained by expression in these cells of potassium channels that are inappropriately opened at hyperpolarized potentials, causing decreased excitability due to increased potassium conductance.
Johnstone
D B
DB
Department of Genetics, University of Washington, Seattle 98195, USA.
Wei
A
A
Butler
A
A
Salkoff
L
L
Thomas
J H
JH
D000818:Animals; D001483:Base Sequence; D005796:Genes / Q000235:genetics*; D008564:Membrane Potentials / Q000502:physiology*; D008969:Molecular Sequence Data; D009154:Mutation / Q000235:genetics*; D009865:Oocytes; D018408:Patch-Clamp Techniques; D010641:Phenotype; D015221:Potassium Channels / Q000235:genetics*; D014981:Xenopus
D015221:Potassium Channels