{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T19:00:37Z","timestamp":1791226837179,"version":"4.1.0"},"reference-count":27,"publisher":"National Academy of Sciences","issue":"6","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[1997,3,18]]},"abstract":"<jats:p>\n                    The proper guidance of the\n                    <jats:italic>Caenorhabditis elegans<\/jats:italic>\n                    hermaphrodite sex myoblasts (SMs) requires the genes\n                    <jats:italic>egl-15<\/jats:italic>\n                    and\n                    <jats:italic>egl-17. egl-15<\/jats:italic>\n                    has been shown to encode the\n                    <jats:italic>C. elegans<\/jats:italic>\n                    orthologue of the fibroblast growth factor receptor (FGFR). Here we clone\n                    <jats:italic>egl-17<\/jats:italic>\n                    and show it to be a member of the fibroblast growth factor (FGF) family, one of the first functional invertebrate FGFs known.\n                    <jats:italic>egl-17<\/jats:italic>\n                    shares homology with other FGF members, conserving the key residues required to form the distinctive tertiary structure common to FGFs. Genetic and molecular evidence demonstrates that the SM migration defect seen in\n                    <jats:italic>egl-17<\/jats:italic>\n                    mutant animals represents complete loss of\n                    <jats:italic>egl-17<\/jats:italic>\n                    function. While mutations in\n                    <jats:italic>egl-17<\/jats:italic>\n                    affect only SM migration, mutations in\n                    <jats:italic>egl-15<\/jats:italic>\n                    can result in larval arrest, scrawny body morphology, and the ability to suppress mutations in\n                    <jats:italic>clr-1<\/jats:italic>\n                    . We propose that EGL-17 (FGF) acts as a ligand for EGL-15 (FGFR) specifically during SM migration and that another ligand(s) activates EGL-15 for its other functions.\n                  <\/jats:p>","DOI":"10.1073\/pnas.94.6.2433","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:35:50Z","timestamp":1027679750000},"page":"2433-2437","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":115,"title":["<i>egl-17<\/i>\n                    encodes an invertebrate fibroblast growth factor family member required specifically for sex myoblast migration in\n                    <i>Caenorhabditis\u2009elegans<\/i>"],"prefix":"10.1073","volume":"94","author":[{"given":"Rebecca D.","family":"Burdine","sequence":"first","affiliation":[{"name":"Departments of Cell Biology, Biology, and Genetics, Yale University, P.O. Box 208005, New Haven, CT 06520-8005"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Estella B.","family":"Chen","sequence":"additional","affiliation":[{"name":"Departments of Cell Biology, Biology, and Genetics, Yale University, P.O. Box 208005, New Haven, CT 06520-8005"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shing F.","family":"Kwok","sequence":"additional","affiliation":[{"name":"Departments of Cell Biology, Biology, and Genetics, Yale University, P.O. Box 208005, New Haven, CT 06520-8005"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael J.","family":"Stern","sequence":"additional","affiliation":[{"name":"Departments of Cell Biology, Biology, and Genetics, Yale University, P.O. 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