Behavioral defects in C. elegans egl-36 mutants result from potassium channels shifted in voltage-dependence of activation

Neuron. 1997 Jul;19(1):151-64. doi: 10.1016/s0896-6273(00)80355-4.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Base Sequence
  • Genes / genetics*
  • Membrane Potentials / physiology*
  • Molecular Sequence Data
  • Mutation / genetics*
  • Oocytes
  • Patch-Clamp Techniques
  • Phenotype
  • Potassium Channels / genetics*
  • Xenopus

Substances

  • Potassium Channels

Associated data

  • GENBANK/AF005246