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1: Dev Biol. 2007 Jul 15;307(2):300-13. Epub 2007 May 6.

FGF9 regulates early hypertrophic chondrocyte differentiation and skeletal
vascularization in the developing stylopod.

Hung IH, Yu K, Lavine KJ, Ornitz DM.

Department of Molecular Biology and Pharmacology, Washington University School of
Medicine, Campus Box 8103, 660 S. Euclid Avenue, St. Louis, MO 63110, USA.

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.

PMID: 17544391 [PubMed - indexed for MEDLINE]

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