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

Duncan B. Johnstone, Aguan Wei, Alice Butler, Lawrence Salkoff, James H. Thomas

Research output: Contribution to journalArticle

40 Scopus citations

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.

Original languageEnglish
Pages (from-to)151-164
Number of pages14
JournalNeuron
Volume19
Issue number1
DOIs
StatePublished - Jul 1997

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