TGFbeta-mediated FGF signaling is crucial for regulating cranial neural crest cell proliferation during frontal bone development. Export

@article{citeulike:5491405, abstract = {The murine frontal bone derives entirely from the cranial neural crest (CNC) and consists of the calvarial (lateral) aspect that covers the frontal lobe of brain and the orbital aspect that forms the roof of bony orbit. TGFbeta and FGF signaling have important regulatory roles in postnatal calvarial development. Our previous study has demonstrated that conditional inactivation of Tgfbr2 in the neural crest results in severe defects in calvarial development, although the cellular and molecular mechanisms by which TGFbeta signaling regulates the fate of CNC cells during frontal bone development remain unknown. Here, we show that TGFbeta IIR is required for proliferation of osteoprogenitor cells in the CNC-derived frontal bone anlagen. FGF acts downstream of TGFbeta signaling in regulating CNC cell proliferation, and exogenous FGF2 rescues the cell proliferation defect in the frontal primordium of Tgfbr2 mutant. Furthermore, the CNC-derived frontal primordium requires TGFbeta IIR to undergo terminal differentiation. However, this requirement is restricted to the developing calvarial aspect of the frontal bone, whereas the orbital aspect forms despite the ablation of Tgfbr2 gene, implying a differential requirement for TGFbeta signaling during the development of various regions of the frontal bone. This study demonstrates the biological significance of TGFbeta-mediated FGF signaling cascade in regulating frontal bone development, suggests that TGFbeta functions as a morphogen in regulating the fate of the CNC-derived osteoblast and provides a model for investigating abnormal craniofacial development.}, author = {Sasaki, Tomoyo and Ito, Yoshihiro and Bringas, Pablo and Chou, Stanley and Urata, Mark M. and Slavkin, Harold and Chai, Yang}, citeulike-article-id = {5491405}, citeulike-linkout-0 = {http://dx.doi.org/10.1242/dev.02200}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/16368934}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=16368934}, doi = {10.1242/dev.02200}, issn = {0950-1991}, journal = {Development (Cambridge, England)}, keywords = {bone, fgf, frontal, neural\_crest\_cells, proliferation, tgfb}, month = {January}, number = {2}, pages = {371--381}, posted-at = {2009-08-20 17:30:33}, priority = {2}, title = {TGFbeta-mediated FGF signaling is crucial for regulating cranial neural crest cell proliferation during frontal bone development.}, url = {http://dx.doi.org/10.1242/dev.02200}, volume = {133}, year = {2006} }

TY - JOUR ID - citeulike:5491405 L3 - citeulike-article-id:5491405 N2 - The murine frontal bone derives entirely from the cranial neural crest (CNC) and consists of the calvarial (lateral) aspect that covers the frontal lobe of brain and the orbital aspect that forms the roof of bony orbit. TGFbeta and FGF signaling have important regulatory roles in postnatal calvarial development. Our previous study has demonstrated that conditional inactivation of Tgfbr2 in the neural crest results in severe defects in calvarial development, although the cellular and molecular mechanisms by which TGFbeta signaling regulates the fate of CNC cells during frontal bone development remain unknown. Here, we show that TGFbeta IIR is required for proliferation of osteoprogenitor cells in the CNC-derived frontal bone anlagen. FGF acts downstream of TGFbeta signaling in regulating CNC cell proliferation, and exogenous FGF2 rescues the cell proliferation defect in the frontal primordium of Tgfbr2 mutant. Furthermore, the CNC-derived frontal primordium requires TGFbeta IIR to undergo terminal differentiation. However, this requirement is restricted to the developing calvarial aspect of the frontal bone, whereas the orbital aspect forms despite the ablation of Tgfbr2 gene, implying a differential requirement for TGFbeta signaling during the development of various regions of the frontal bone. This study demonstrates the biological significance of TGFbeta-mediated FGF signaling cascade in regulating frontal bone development, suggests that TGFbeta functions as a morphogen in regulating the fate of the CNC-derived osteoblast and provides a model for investigating abnormal craniofacial development. IS - 2 JF - Development (Cambridge, England) SN - 0950-1991 EP - 381 TI - TGFbeta-mediated FGF signaling is crucial for regulating cranial neural crest cell proliferation during frontal bone development. VL - 133 SP - 371 KW - bone KW - fgf KW - frontal KW - neural_crest_cells KW - proliferation KW - tgfb AU - Sasaki, Tomoyo AU - Ito, Yoshihiro AU - Bringas, Pablo AU - Chou, Stanley AU - Urata, Mark AU - Slavkin, Harold AU - Chai, Yang PY - 2006/01// UR - http://dx.doi.org/10.1242/dev.02200 ER -