The International Journal of Developmental Biology

Int. J. Dev. Biol. 42: 817 - 820 (1998)

Vol 42, Issue 6

Immunohistochemical localization of TGF-beta type II receptor and TGF-beta3 during palatogenesis in vivo and in vitro

Published: 1 September 1998

X M Cui, D Warburton, J Zhao, D L Crowe and C F Shuler

The University of Southern California, School of Dentistry, Center for Craniofacial Molecular Biology, Los Angeles 90033, USA.

Abstract

The disappearance of medial edge epithelium (MEE) is a critical event for palate fusion. TGF-beta3 is one factor participating in the regulation of this process. To investigate the nature of ligand-receptor interactions in vivo between TGF-beta3 and the type II TGF-beta receptor (TbetaR-II), we compared the expression pattern of the receptor with TGF-beta3. Immunohistochemical analysis of the mouse fetus from E12 to E15 showed that expression of TbetaR-II in the palate began at E13 when the palatal shelves were in a vertical orientation. TbetaR-II was localized in the epithelial cells. This epithelium-favored distribution remained during palatal shelf elevation, the medial edge epithelial adherence, and midline epithelial seam disruption. After palate fusion and mesenchyme confluence, weak expression of TbetaR-II was present in the mesenchyme. To verify the possibility that TGF-beta3 and TbetaR-II expression coincide, immunohistochemistry was used to localize them both in serial sections. The distribution pattern of TGF-beta3 was also epithelium-limited in the palate from E13 to E15, and the spatial localization was correlated with the expression of TbetaR-II. Immunohistochemical localization of TbetaR-II and TGF-beta3 in palatal shelves in organ culture had patterns that were consistent with the in vivo results. These results suggest that TGF-beta3 exerts its developmental role through TbetaR-II in an autocrine fashion. The expression of both TGF-beta3 and TbetaR-II was below the detectable level in the mesenchyme following MEE disruption, suggesting that the TGF-beta3 signal might not be required once the MEE has completed phenotypic transformation/migration.

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