Journal
DEVELOPMENTAL BIOLOGY
Volume 307, Issue 2, Pages 300-313Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2007.04.048
Keywords
fibroblast growth factor 9 (FGF9); skeletal development; growth plate; chondrocyte; osteoblast; periosteum; perichondrium; vascular development
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Funding
- NICHD NIH HHS [HD049808, T32 HD043010-05, K08 HD058219, 1-T32-HD043010, R01 HD049808, R01 HD049808-02, T32 HD043010] Funding Source: Medline
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Gain-of-function mutations in fibroblast growth factor (FGF) receptors result in chondrodysplasia and craniosynostosis syndromes, highlighting the critical role for FGF signaling in skeletal development. Although the FGFRs involved in skeletal development have been well characterized, only a single FGF ligand, FGF18, has been identified that regulates skeletal development during embryogenesis. Here we identify Fgf9 as a second FGF ligand that is critical for skeletal development. We show that Fgf9 is expressed in the proximity of developing skeletal elements and that Fgf9-deficient mice exhibit rhizomelia (a disproportionate shortening of proximal skeletal elements), which is a prominent feature of patients with FGFR3-induced chondrodysplasia syndromes. Although Fgf9 is expressed in the apical ectodermal ridge in the limb bud, we demonstrate that the Fgf9(-/-) limb phenotype results from loss of FGF9 functions after formation of the mesenchymal condensation. In developing stylopod elements, FGF9 promotes chondrocyte hypertrophy at early stages and regulates vascularization of the growth plate and osteogenesis at later stages of skeletal development. (c) 2007 Elsevier Inc. All rights reserved.
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