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Article

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

Neuron - 1 Jul 1997

Johnstone D B, Wei A, Butler A, Salkoff L, Thomas J H

Abstract excerpt

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...

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PMID: 9247271
DOI: 10.1016/s0896-6273(00)80355-4

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

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