{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T15:00:16Z","timestamp":1791039616087,"version":"4.1.0"},"reference-count":89,"publisher":"The Company of Biologists","issue":"19","license":[{"start":{"date-parts":[[2004,4,1]],"date-time":"2004-04-01T00:00:00Z","timestamp":1080777600000},"content-version":"vor","delay-in-days":183,"URL":"http:\/\/www.biologists.com\/user-licence-1-1"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2003,10,1]]},"abstract":"<jats:p>The extent to which excitable cells and behavior modulate animal development has not been examined in detail. Here, we demonstrate the existence of a novel pathway for promoting vulval fates in C. elegansthat involves activation of the heterotrimeric G\u03b1q protein, EGL-30. EGL-30 acts with muscle-expressed EGL-19 L-type voltage-gated calcium channels to promote vulva development, and acts downstream or parallel to LET-60 (RAS). This pathway is not essential for vulval induction on standard Petri plates,but can be stimulated by expression of activated EGL-30 in neurons, or by an EGL-30-dependent change in behavior that occurs in a liquid environment. Our results indicate that excitable cells and animal behavior can provide modulatory inputs into the effects of growth factor signaling on cell fates,and suggest that communication between these cell populations is important for normal development to occur under certain environmental conditions.<\/jats:p>","DOI":"10.1242\/dev.00670","type":"journal-article","created":{"date-parts":[[2003,8,18]],"date-time":"2003-08-18T22:40:51Z","timestamp":1061246451000},"page":"4553-4566","source":"Crossref","is-referenced-by-count":31,"title":["Modulation of EGF receptor-mediated vulva development by the heterotrimeric G-protein G\u03b1q and excitable cells in<i>C<\/i>.<i>elegans<\/i>"],"prefix":"10.1242","volume":"130","author":[{"given":"Nadeem","family":"Moghal","sequence":"first","affiliation":[{"name":"Howard Hughes Medical Institute and Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L. Rene","family":"Garcia","sequence":"additional","affiliation":[{"name":"Department of Biology, Texas A&M University, 3258 TAMU, College Station,TX 77843, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liakot A.","family":"Khan","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Neurobiology, Neuroscience Research Institute AIST,Tsukuba, 305-8566, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kouichi","family":"Iwasaki","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Neurobiology, Neuroscience Research Institute AIST,Tsukuba, 305-8566, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul W.","family":"Sternberg","sequence":"additional","affiliation":[{"name":"Howard Hughes Medical Institute and Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","reference":[{"key":"2021042604331756600_REF1","doi-asserted-by":"crossref","unstructured":"Aroian, R. and Sternberg, P. 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