Roles of FGFR3 during morphogenesis of Meckel's cartilage and mandibular bones.

To address the functions of FGFR2 and FGFR3 signaling during mandibular skeletogenesis, we over-expressed in the developing chick mandible, replication-competent retroviruses carrying truncated FGFR2c or FGFR3c that function as dominant negative receptors (RCAS-dnFGFR2 and RCAS-dnFGFR3). Injection of RCAS-dnFGFR3 between HH15 and 20 led to reduced proliferation, increased apoptosis, and decreased differentiation of chondroblasts in Meckel's cartilage. These changes resulted in the formation of a hypoplastic mandibular process and truncated Meckel's cartilage.

FGF signaling in mandibular skeletogenesis.

Objective: To examine the functions of FGF/FGFR signaling during mandibular skeletogenesis in ovo.

Design: We examined the effects of inhibition of FGF signaling during mandibular skeletogenesis by overexpressing replication-competent RCAS virus encoding a truncated form of FGFR3 in the chicken mandibular process between stages 17 and 26.

Results: Injection of RCAS-dnFGFR3 into the developing mandible resulted in abnormalities in a stage- and region-dependent manner.

Tissue-specific expression of Fgfr2b and Fgfr2c isoforms, Fgf10 and Fgf9 in the developing chick mandible.

Experimental evidence has demonstrated the importance of FGF signalling in morphogenesis of the mandibular processes. FGFs transmit their signals through four tyrosine kinase transmembrane receptors (FGFRs). Alternative splicing in FGFRs including FGFR2 generates different isoforms that exhibit different ligand-specificities, exclusive tissue distributions and specific biological functions.