Plastic Surgery Research Council
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NON-CANONICAL TGF≤? SIGNALING REGULATES TONGUE DEVELOPMENT
Presenter: Akiko Suzuki, DDS, PhD
Co-Authors: Iwata J; Sanchez-Lara PA; Urata M; Chai Y
University of Southern California

Microglossia is one of the common congenital birth defects in humans and adversely impacts quality of life. In vertebrates, tongue muscle derives from cranial mesoderm, whereas skeletal elements, tendons, and connective tissue in the craniofacial region originate from cranial neural crest (CNC) cells. Loss of transforming growth factor beta (TGF≤≤) type II receptor in CNC cells in mice (TGF≤br2fl/fl;Wnt1-Cre) causes microglossia. However, it is still unclear how TGF≤≤ signaling in CNC cells regulates the fate of mesoderm derived myoblasts. We show that loss of TGF≤≤ signaling results in a failure of CNC derived fibroblast differentiation, followed by a disruption of TGF≤? mediated expression of both bone morphogenic proteins (BMPs) and fibroblastic growth factors (FGFs) and decreased myogenic cell proliferation and differentiation activities. Exogenous BMPs and FGFs can restore cell proliferation and differentiation in the tongue of TGF≤br2fl/fl;Wnt1-Cre mice. Thus, CNC derived fibroblasts regulate mesoderm derived myoblasts via TGF≤? mediated BMP and FGF signaling during tongue development. Supported by NIDCR. R01 DE014078, DE 012711.


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