p38 mitogen-activated protein kinase/Hog1p regulates translation of the AU-rich-element-bearing MFA2 transcript.
p38 mitogen-activated protein kinase/Hog1p regulates translation of the AU-rich-element-bearing MFA2 transcript.
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p38 丝裂原激活蛋白激酶/Hog1p 调节富含 AU 元素的 MFA2 转录物的翻译。
DOI：
10.1128/mcb.25.22.9753-9763.2005
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发表时间：
2005
影响因子：
5.3
通讯作者：
Peltz,StuartW
中科院分区：
文献类型：
--
作者：
Vasudevan,Shobha;Garneau,Nicole;TuKhounh,Danny;Peltz,StuartW
富Au元素(ARE)通过p38丝裂原活化蛋白激酶(MAPK)/Hog1p通路调节酿酒酵母对外界和内部刺激的反应。我们证明了含Are的MFA2 3‘非翻译区(UTR)以p38MAPK/Hog1p依赖的方式控制翻译效率，以响应碳源生长条件。碳源对MFA2 3‘-UTR控制的翻译的调节作用涉及保守的ARE结合蛋白、与CaP/eIF4G复合体相互作用的ELAV/TIA-1类Pub1p和翻译/mRNA稳定因子Poly(A)结合蛋白(Pab1p)的作用。根据碳源生长条件，Pub1p以p38MAPK/Hog1p调控的方式与MFA2 3‘-UTR结合。值得注意的是，p38MAPK/Hog1p也需要对Pab1p进行调节以响应碳源。我们发现Pab1p能以调节的方式结合MFA2 3‘-UTR，从而控制MFA2 3’-UTR报告基因的翻译。全长Pab1p与MFA2 3‘-UTR的结合与翻译抑制有关。重要的是，Pab1p只在PUB1菌株中与MFA2 3‘-UTR结合，并且与这一要求相关，Pub1p以碳源/Hog1p调节的方式控制MFA2的翻译抑制。这些结果表明，p38MAPK/Hog1p通路通过调节Pab1p和Pub1p的募集来调节3‘-UTR介导的翻译，Pab1p和Pub1p可以与翻译机制相互作用。
AU-rich-element (ARE)-mediated mRNA regulation occurs inSaccharomyces cerevisiaein response to external and internal stimuli through the p38 mitogen-activated protein kinase (MAPK)/Hog1p pathway. We demonstrate that the ARE-bearing MFA2 3′ untranslated region (UTR) controls translation efficiency in a p38 MAPK/Hog1p-dependent manner in response to carbon source growth conditions. The carbon source-regulated effect on MFA2 3′-UTR-controlled translation involves the role of conserved ARE binding proteins, the ELAV/TIA-1-like Pub1p, which can interact with the cap/eIF4G complex, and the translation/mRNA stability factor poly(A) binding protein (Pab1p). Pub1p binds the MFA2 3′-UTR in a p38 MAPK/Hog1p-regulated manner in response to carbon source growth conditions. Significantly, the p38 MAPK/Hog1p is also required to modulate Pab1p in response to carbon source. We find that Pab1p can bind the MFA2 3′-UTR in a regulated manner to control MFA2 3′-UTR reporter translation. Binding of full-length Pab1p to the MFA2 3′-UTR correlates with translation repression. Importantly, Pab1p binds the MFA2 3′-UTR only in aPUB1strain, and correlating with this requirement, Pub1p controls translation repression of MFA2 in a carbon source/Hog1p-regulated manner. These results suggest that the p38 MAPK/Hog1p pathway regulates 3′-UTR-mediated translation by modulating recruitment of Pab1p and Pub1p, which can interact with the translation machinery.