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响应错义翻译增加而诱导热休克调节子需要对畸形蛋白质进行氧化修饰。

Induction of the heat shock regulon in response to increased mistranslation requires oxidative modification of the malformed proteins.

作者信息

Fredriksson Asa, Ballesteros Manuel, Dukan Sam, Nyström Thomas

机构信息

Department of Cell and Molecular Biology - Microbiology, Göteborg University, Medicinaregatan 9C, 413 90 Göteborg, Sweden.

出版信息

Mol Microbiol. 2006 Jan;59(1):350-9. doi: 10.1111/j.1365-2958.2005.04947.x.

DOI:10.1111/j.1365-2958.2005.04947.x
PMID:16359340
Abstract

The Escherichia coli rpsD12 allele, which reduces translational fidelity and elevates expression of heat shock protein (Hsp) genes, only enhanced Hsp gene expression in the presence of oxygen. Similarly, the rpsL141 allele, which reduces mistranslation and Hsp gene expression, failed to affect the Hsp regulon in cells grown anaerobically. Increased production of Hsps in response to starvation is associated with increased mistranslation and was demonstrated to likewise require the presence of oxygen. Thus, mistranslation triggered by starvation or mutations in the accuracy centre of the ribosome appear to elevate Hsp gene expression via an oxidative modification of mistranslated proteins. In contrast, Hsp gene induction during temperature upshifts was independent of oxygen availability. The data further suggest that it is the oxidative modification of mistranslated DnaK substrates rather than oxidation of DnaK itself that triggers Hsp gene expression upon starvation.

摘要

大肠杆菌的rpsD12等位基因可降低翻译保真度并提高热休克蛋白(Hsp)基因的表达,但其仅在有氧条件下增强Hsp基因的表达。同样,降低错义翻译和Hsp基因表达的rpsL141等位基因,在厌氧生长的细胞中未能影响Hsp调节子。饥饿时Hsp产量增加与错义翻译增加相关,并且同样被证明需要有氧存在。因此,饥饿或核糖体准确性中心的突变引发的错义翻译似乎通过错义翻译蛋白质的氧化修饰来提高Hsp基因的表达。相比之下,温度升高期间的Hsp基因诱导与氧气供应无关。数据进一步表明,是错义翻译的DnaK底物的氧化修饰而非DnaK本身的氧化触发了饥饿时的Hsp基因表达。

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