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In addition, we showed that human CYP26B1 null patients have more severe and seemingly opposite skull defects, characterized by smaller and fragmented calvaria, while the cellular basis of these defects remained largely unclear. Here, treating juvenile zebrafish with exogenous RA or a chemical Cyp26 inhibitor in the presence or absence of osteogenic cells or bone-resorbing osteoclasts, we demonstrate that both reduced calvarial size and calvarial fragmentation are also caused by RA-induced premature osteoblast-to-preosteocyte transitioning. During calvarial growth, the resulting osteoblast deprival leads to decreased osteoid production and thereby smaller and thinner calvaria, while calvarial fragmentation is caused by increased osteoclast stimulation through the gained preosteocytes. Together, our data demonstrate that RA-induced osteoblast-to-preosteocyte transitioning has multiple effects on developing bone in Cyp26b1 mutants, ranging from gain to loss of bone, and depending on the allelic strength, the developmental stage and the cellular context.<\/jats:p>","DOI":"10.1242\/dev.129189","type":"journal-article","created":{"date-parts":[[2016,2,23]],"date-time":"2016-02-23T03:24:13Z","timestamp":1456197853000},"source":"Crossref","is-referenced-by-count":15,"title":["Retinoic acid-induced premature osteoblast-to-preosteocyte transitioning has multiple effects on calvarial development"],"prefix":"10.1242","author":[{"given":"Shirine","family":"Jeradi","sequence":"first","affiliation":[{"name":"Institute of Developmental Biology, University of Cologne, Cologne, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthias","family":"Hammerschmidt","sequence":"additional","affiliation":[{"name":"Institute of Developmental Biology, University of Cologne, Cologne, Germany"},{"name":"Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany"},{"name":"Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","reference":[{"key":"2021042608465829500_DEV129189C1","doi-asserted-by":"publisher","first-page":"811","DOI":"10.1242\/dmm.015693","article-title":"Zebrafish enpp1 mutants exhibit pathological mineralization, mimicking features of generalized arterial calcification of infancy (GACI) and pseudoxanthoma elasticum (PXE)","volume":"7","author":"Apschner","year":"2014","journal-title":"Dis. 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