Abstract:
:Smad4 is a central intracellular effector of TGF-beta signaling. Smad-independent TGF-beta 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-beta 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-beta signaling in diverse contexts during embryonic organogenesis. The ability of epithelium to utilize both pathways illustrates the complicated nature of TGF-beta signaling mechanisms in development and disease.
journal_name
Dev Celljournal_title
Developmental cellauthors
Xu X,Han J,Ito Y,Bringas P Jr,Deng C,Chai Ydoi
10.1016/j.devcel.2008.06.004subject
Has Abstractpub_date
2008-08-01 00:00:00pages
322-9issue
2eissn
1534-5807issn
1878-1551pii
S1534-5807(08)00245-1journal_volume
15pub_type
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