The International Journal of Developmental Biology

Int. J. Dev. Biol. 44: 397 - 402 (2000)

Vol 44, Issue 4

The TGF-beta type III receptor is localized to the medial edge epithelium during palatal fusion

Published: 30 November -0001

X M Cui and C F Shuler

The University of Southern California, School of Dentistry, Center for Craniofacial Molecular Biology, Los Angeles 90089, USA.


During palatal fusion, the medial edge epithelial cells (MEE) but not the oral/nasal palatal epithelium, selectively undergo epithelial-mesenchymal transformation. It is known that this process is regulated, at least in part, by endogenous TGF-beta3. One conceivable mechanism is that restricted expression of TGF-beta receptors (TbetaRs) in a subpopulation of cells may localize TGF-beta responsiveness (Brown et al., 1999). However, TGF-beta type II receptor (TbetaR-II) is expressed by all palatal epithelial cells during palatal fusion (Cui et al., 1998) and therefore cannot localize TGF-beta3 responsiveness. To investigate the role of TGF-beta type III receptor (TbetaR-III) in MEE transformation, we examined the expression pattern of TbetaR-III in the developing palate from E12 to E15 mice in vivo and in vitro by immunohistochemistry and compared the expression pattern to that of type I receptor (TbetaR-I). The expression of TbetaR-III was temporo-spatially restricted to the MEE during palatal fusion, while the expression of TbetaR-I was primarily localized in all palatal epithelia, consistent with the expression patterns of TbetaR-II and TGF-beta3 (Cui et al., 1998). These results support our hypothesis that TbetaR-III localizes and mediates the developmental role of TGF-beta3 on MEE transformation by specific expression in the MEE. TbetaR-III may modulate TGF-beta3 binding to TbetaR-II in the MEE cells to locally enhance TGF-beta3 autocrine signaling through the TbetaR-I/TbetaR-II receptor complex, which contributes to MEE selective epithelial-mesenchymal transformation.

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