title: The SLO-1 BK channel of Caenorhabditis elegans is critical for muscle function and is involved in dystrophin-dependent muscle dystrophy.
abstract: The Caenorhabditis elegans SLO-1 channel belongs to the family of calcium-activated large conductance BK potassium channels. SLO-1 has been shown to be involved in neurotransmitter release and ethanol response. Here, we report that SLO-1 also has a critical role in muscles. Inactivation of the slo-1 gene in muscles leads to phenotypes similar to those caused by mutations of the dystrophin homologue dys-1. Notably, slo-1 mutations result in a progressive muscle degeneration when put into a sensitized genetic background. slo-1 localization was observed by gfp reporter gene in both the M-line and the dense bodies (Z line) of the C.elegans body-wall muscles. Using the inside-out configuration of the patch clamp technique on body-wall muscle cells of acutely dissected wild-type worms, we characterized a Ca2+-activated K+ channel that was identified unambiguously as SLO-1. Since neither the abundance nor the conductance of SLO-1 was changed significantly in dys-1 mutants compared to wild-type animals, it is likely that the inactivation of dys-1 causes a misregulation of SLO-1. All in all, these results indicate that SLO-1 function in C.elegans muscles is related to the dystrophin homologue DYS-1.
authors.affiliation: CGMC, CNRS-UMR 5534, Université C. Bernard Lyon-1, 69622 Villeurbanne, France.
authors.forename: Maité
authors.initials: M
authors.lastname: Carre-Pierrat
authors.forename: Karine
authors.initials: K
authors.lastname: Grisoni
authors.forename: Kathrin
authors.initials: K
authors.lastname: Gieseler
authors.forename: Marie-Christine
authors.initials: MC
authors.lastname: Mariol
authors.forename: Edwige
authors.initials: E
authors.lastname: Martin
authors.forename: Maelle
authors.initials: M
authors.lastname: Jospin
authors.forename: Bruno
authors.initials: B
authors.lastname: Allard
authors.forename: Laurent
authors.initials: L
authors.lastname: Ségalat
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D017173:Caenorhabditis elegans / Q000378:metabolism*; D029742:Caenorhabditis elegans Proteins / Q000378:metabolism / Q000502:physiology*; D016189:Dystrophin / Q000378:metabolism*; D051036:Large-Conductance Calcium-Activated Potassium Channels / Q000502:physiology*; D009132:Muscles / Q000378:metabolism* / Q000473:pathology; D009137:Muscular Dystrophy, Animal / Q000378:metabolism* / Q000473:pathology; D009154:Mutation / Q000235:genetics; D010641:Phenotype; D024681:Potassium Channels, Calcium-Activated / Q000378:metabolism
chemical_list: D029742:Caenorhabditis elegans Proteins; D016189:Dystrophin; D051036:Large-Conductance Calcium-Activated Potassium Channels; D024681:Potassium Channels, Calcium-Activated; C406103:dys-1 protein, C elegans; C494845:slo-1 protein, C elegans