{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T20:36:23Z","timestamp":1772138183302,"version":"3.50.1"},"reference-count":38,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2009,2,9]],"date-time":"2009-02-09T00:00:00Z","timestamp":1234137600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Exp Zool Pt B"],"published-print":{"date-parts":[[2009,6,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Fibroblast growth factor receptor 2 (Fgfr2) has two splice variants IIIb and IIIc, which are unique in function and localization. Signalling through Fgfr2IIIb controls epithelial\u2013mesenchymal interactions, which regulate morphogenesis during the development of several organs including the palate and tooth. In this study, we confirm that molar tooth development in <jats:italic>Fgfr2IIIb<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice is arrested early in development and that the molar teeth of <jats:italic>Fgf10<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice develop through all the normal stages of morphogenesis. We show that the molar phenotype of <jats:italic>Fgfr2IIIb<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic> mice is, in part, owing to reduced cell proliferation in both epithelial and mesenchymal compartments. We also show that the developing molar teeth of <jats:italic>Fgf10<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice exhibit reduced cell proliferation. However, this reduction is not sufficient to arrest molar development.<\/jats:p><jats:p>Recent evidence has indicated that Fgfr2IIIb\/Fgf10 signalling is active in the calvaria in some pathological situations as heterozygous deletion of <jats:italic>Fgfr2<\/jats:italic> exon <jats:italic>IIIc<\/jats:italic> in mice leads to ectopic expression of <jats:italic>Fgfr2IIIb<\/jats:italic> in the calvarial bones and causes craniosynostosis. Here, we investigate the mRNA expression of <jats:italic>Fgfr2IIIb<\/jats:italic> and <jats:italic>Fgfr2IIIc<\/jats:italic> as well as their ligands <jats:italic>Fgf3<\/jats:italic>, \u2212<jats:italic>7<\/jats:italic> and \u2212<jats:italic>10<\/jats:italic> in the developing murine tooth, palate and calvaria. We show that <jats:italic>Fgf7<\/jats:italic> is expressed in the calvarial mesenchyme adjacent to the developing frontal bone and <jats:italic>Fgf10<\/jats:italic> is expressed by osteoprogenitors in the developing frontal bone condensation. Taken together, we highlight the overlapping roles of Fgfr2IIIb\/Fgf10 signalling in controlling epithelial\u2013mesenchymal interactions during normal palate and tooth morphogenesis and how elevated signalling through Fgfr2IIIb\/Fgf10 solely within the mesenchyme can result in abnormal calvarial morphogenesis. <jats:italic>J. Exp. Zool. (Mol. Dev. Evol.) 312B:351\u2013360, 2009<\/jats:italic>. \u00a9 2009 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jez.b.21276","type":"journal-article","created":{"date-parts":[[2009,2,9]],"date-time":"2009-02-09T20:04:19Z","timestamp":1234209859000},"page":"351-360","source":"Crossref","is-referenced-by-count":17,"title":["Convergent signalling through Fgfr2 regulates divergent craniofacial morphogenesis"],"prefix":"10.1002","volume":"312B","author":[{"given":"Lotta","family":"Veistinen","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas","family":"\u00c5berg","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David 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