{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T03:14:17Z","timestamp":1787022857124,"version":"build-2736575974"},"reference-count":80,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2012,3,1]],"date-time":"2012-03-01T00:00:00Z","timestamp":1330560000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2012,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Variations in K+ channel composition allow for differences in cell excitability and, at an organismal level, provide flexibility to behavioral regulation. When the function of a K+ channel is disrupted, the remaining K+ channels might incompletely compensate, manifesting as abnormal organismal behavior. In this study, we explored how different K+ channels interact to regulate the neuromuscular circuitry used by Caenorhabditis elegans males to protract their copulatory spicules from their tail and insert them into the hermaphrodite\u2019s vulva during mating. We determined that the big current K+ channel (BK)\/SLO-1 genetically interacts with ether-a-go-go (EAG)\/EGL-2 and EAG-related gene\/UNC-103 K+ channels to control spicule protraction. Through rescue experiments, we show that specific slo-1 isoforms affect spicule protraction. Gene expression studies show that slo-1 and egl-2 expression can be upregulated in a calcium\/calmodulin-dependent protein kinase II-dependent manner to compensate for the loss of unc-103 and conversely, unc-103 can partially compensate for the loss of SLO-1 function. In conclusion, an interaction between BK and EAG family K+ channels produces the muscle excitability levels that regulate the timing of spicule protraction and the success of male mating behavior.<\/jats:p>","DOI":"10.1534\/genetics.111.137455","type":"journal-article","created":{"date-parts":[[2011,12,15]],"date-time":"2011-12-15T22:48:28Z","timestamp":1323989308000},"page":"1025-1041","source":"Crossref","is-referenced-by-count":22,"title":["Cell Excitability Necessary for Male Mating Behavior in\n                    <i>Caenorhabditis elegans<\/i>\n                    Is Coordinated by Interactions Between Big Current and Ether-A-Go-Go Family K+ Channels"],"prefix":"10.1093","volume":"190","author":[{"given":"Brigitte","family":"LeBoeuf","sequence":"first","affiliation":[{"name":"Howard Hughes Medical Institute, Department of Biology, Texas A&M University, College Station, Texas 77843"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L Rene","family":"Garcia","sequence":"additional","affiliation":[{"name":"Howard Hughes Medical Institute, Department of Biology, Texas A&M University, College Station, Texas 77843"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2012,3,1]]},"reference":[{"key":"2022011219162365300_bib1"},{"key":"2022011219162365300_bib2","doi-asserted-by":"crossref","first-page":"1853","DOI":"10.1172\/JCI27438","article-title":"CaM kinase II selectively signals to histone deacetylase 4 during cardiomyocyte hypertrophy","volume":"116","author":"Backs","year":"2006","journal-title":"J. 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