{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T11:31:06Z","timestamp":1791804666972,"version":"4.3.4"},"reference-count":48,"publisher":"The Company of Biologists","issue":"14","license":[{"start":{"date-parts":[[2019,7,15]],"date-time":"2019-07-15T00:00:00Z","timestamp":1563148800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/www.biologists.com\/user-licence-1-1\/"}],"funder":[{"DOI":"10.13039\/501100000268","name":"Biotechnology and Biological Sciences Research Council","doi-asserted-by":"publisher","award":["BB\/K008668\/1"],"award-info":[{"award-number":["BB\/K008668\/1"]}],"id":[{"id":"10.13039\/501100000268","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000011","name":"Howard Hughes Medical Institute","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000011","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 GM078620"],"award-info":[{"award-number":["R01 GM078620"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000764","name":"Kings College London","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000764","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,7,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>In human, mutations of the protocadherins FAT4 and DCHS1 result in Van Maldergem syndrome, which is characterised, in part, by craniofacial abnormalities. Here, we analyse the role of Dchs1-Fat4 signalling during osteoblast differentiation in mouse. We show that Fat4 and Dchs1 mutants mimic the craniofacial phenotype of the human syndrome and that Dchs1-Fat4 signalling is essential for osteoblast differentiation. In Dchs1\/Fat4 mutants, proliferation of osteoprogenitors is increased and osteoblast differentiation is delayed. We show that loss of Dchs1-Fat4 signalling is linked to increased Yap-Tead activity and that Yap is expressed and required for proliferation in osteoprogenitors. In contrast, Taz is expressed in more-committed Runx2-expressing osteoblasts, Taz does not regulate osteoblast proliferation and Taz-Tead activity is unaffected in Dchs1\/Fat4 mutants. Finally, we show that Yap and Taz differentially regulate the transcriptional activity of Runx2, and that the activity of Yap-Runx2 and Taz-Runx2 complexes is altered in Dchs1\/Fat4 mutant osteoblasts. In conclusion, these data identify Dchs1-Fat4 as a signalling pathway in osteoblast differentiation, reveal its crucial role within the early Runx2 progenitors, and identify distinct requirements for Yap and Taz during osteoblast differentiation.<\/jats:p>","DOI":"10.1242\/dev.176776","type":"journal-article","created":{"date-parts":[[2019,7,29]],"date-time":"2019-07-29T10:45:11Z","timestamp":1564397111000},"source":"Crossref","is-referenced-by-count":32,"title":["Dchs1-Fat4 regulation of osteogenic differentiation in mouse"],"prefix":"10.1242","volume":"146","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2967-4554","authenticated-orcid":false,"given":"Ivan","family":"Crespo-Enriquez","sequence":"first","affiliation":[{"name":"Centre for Craniofacial and Regenerative Biology 1 , Faculty of Dentistry, Oral & Craniofacial Sciences , , Floor 27, Guy's Tower, London SE1 9RT , UK"},{"name":"King's College London 1 , Faculty of Dentistry, Oral & Craniofacial Sciences , , Floor 27, Guy's 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