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We isolated dominant, gain-of-function alleles of egl-30 as intragenic revertants of an egl-30 reduction-of-function mutation. Using these gain-of-function mutants and existing reduction-of-function mutants, we examined the site and mode of action of EGL-30. On the basis of pharmacological analysis, it has been determined that egl-30 functions both in the nervous system and in the vulval muscles for egg-laying behavior. Genetic epistasis over mutations that eliminate detectable levels of serotonin reveals that egl-30 requires serotonin to regulate egg laying. Furthermore, pharmacological response assays strongly suggest that EGL-30 may directly couple to a serotonin receptor to mediate egg laying. We also examined genetic interactions with mutations in the gene that encodes the single C. elegans homolog of PLC\u03b2 and mutations in genes that encode signaling molecules downstream of PLC\u03b2. We conclude that PLC\u03b2 functions in parallel with egl-30 with respect to egg laying or is not the major effector of EGL-30. In contrast, PLC\u03b2-mediated signaling is likely downstream of EGL-30 with respect to pharyngeal-pumping behavior. Our data indicate that there are multiple signaling pathways downstream of EGL-30 and that different pathways could predominate with respect to the regulation of different behaviors.<\/jats:p>","DOI":"10.1093\/genetics\/165.4.1805","type":"journal-article","created":{"date-parts":[[2021,4,27]],"date-time":"2021-04-27T15:16:16Z","timestamp":1619536576000},"page":"1805-1822","source":"Crossref","is-referenced-by-count":90,"title":["<i>Caenorhabditis elegans<\/i> G\u03b1q Regulates Egg-Laying Behavior via a PLC\u03b2-Independent and Serotonin-Dependent Signaling Pathway and Likely Functions Both in the Nervous System and in Muscle"],"prefix":"10.1093","volume":"165","author":[{"given":"Carol A","family":"Bastiani","sequence":"first","affiliation":[{"name":"Howard Hughes Medical Institute, Pasadena, California 91125"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shahla","family":"Gharib","sequence":"additional","affiliation":[{"name":"Howard Hughes Medical Institute, Pasadena, California 91125"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melvin I","family":"Simon","sequence":"additional","affiliation":[{"name":"Division of Biology, California Institute of Technology, Pasadena, California 91125"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul W","family":"Sternberg","sequence":"additional","affiliation":[{"name":"Howard Hughes Medical Institute, Pasadena, California 91125"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2003,12,1]]},"reference":[{"key":"2022010522444441700_R1","doi-asserted-by":"crossref","first-page":"5587","DOI":"10.1073\/pnas.88.13.5587","article-title":"G alpha 16, a G protein alpha subunit specifically expressed in hematopoietic cells","volume":"88","author":"Amatruda","year":"1991","journal-title":"Proc. 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