Ectodermal Smad4 and p38 MAPK Are Functionally Redundant in Mediating TGF-β/BMP Signaling during Tooth and Palate Development

107Citations
Citations of this article
36Readers
Mendeley users who have this article in their library.

Abstract

Smad4 is a central intracellular effector of TGF-β signaling. Smad-independent TGF-β pathways, such as those mediated by p38 MAPK, have been identified in cell culture systems, but their in vivo functional mechanisms remain unclear. In this study, we investigated the role of TGF-β signaling in tooth and palate development and noted that conditional inactivation of Smad4 in oral epithelium results in much milder phenotypes than those seen with the corresponding receptor mutants, Bmpr1a and Tgfbr2, respectively. Perturbed p38 function in these tissues likewise has no effect by itself; however, when both Smad4 and p38 functions are compromised, dramatic recapitulation of the receptor mutant phenotypes results. Thus, our study demonstrates that p38 and Smad4 are functionally redundant in mediating TGF-β signaling in diverse contexts during embryonic organogenesis. The ability of epithelium to utilize both pathways illustrates the complicated nature of TGF-β signaling mechanisms in development and disease. © 2008 Elsevier Inc. All rights reserved.

Author supplied keywords

Cite

CITATION STYLE

APA

Xu, X., Han, J., Ito, Y., Bringas, P., Deng, C., & Chai, Y. (2008). Ectodermal Smad4 and p38 MAPK Are Functionally Redundant in Mediating TGF-β/BMP Signaling during Tooth and Palate Development. Developmental Cell, 15(2), 322–329. https://doi.org/10.1016/j.devcel.2008.06.004

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free