Ectodermal Smad4 and p38 MAPK are functionally redundant in mediating TGF-beta/BMP signaling during tooth and palate development.

Ectodermal Smad4 and p38 MAPK are functionally redundant in mediating TGF-beta/BMP signaling during tooth and palate development.
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DOI:
10.1016/j.devcel.2008.06.004
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发表时间:
2008-08
期刊:
影响因子:
11.8
通讯作者:
Chai, Yang
Chai, Yang
中科院分区:
生物学1区
文献类型:
--
作者:
Xu, Xun;Han, Jun;Ito, Yoshihiro;Bringas, Pablo, Jr.;Deng, Chuxia;Chai, Yang

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Smad 4是TGF-β信号传导的中心细胞内效应物。Smad非依赖性TGF-β通路,如p38 MAPK介导的通路,已在细胞培养系统中被鉴定,但其体内功能机制仍不清楚。在这项研究中,我们研究了TGF-β信号在牙齿和腭发育中的作用,并注意到Smad 4在口腔上皮中的条件性失活导致的表型比相应的受体突变体Bmpr 1a和Tgfbr 2分别观察到的表型要温和得多。在这些组织中,扰动的p38功能本身同样没有影响,但是当Smad 4和p38功能都受到损害时,受体突变表型的戏剧性重演结果。因此,我们的研究表明,p38和Smad 4在胚胎器官发生过程中的不同背景下介导TGF-β信号传导是功能冗余的。上皮利用两种途径的能力说明了发育和疾病中TGF-β信号传导机制的复杂性质。
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, but that 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.
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