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ChrR正向调控球形红杆菌细胞色素c2基因的转录。

ChrR positively regulates transcription of the Rhodobacter sphaeroides cytochrome c2 gene.

作者信息

Schilke B A, Donohue T J

机构信息

Department of Bacteriology, University of Wisconsin, Madison 53706, USA.

出版信息

J Bacteriol. 1995 Apr;177(8):1929-37. doi: 10.1128/jb.177.8.1929-1937.1995.

Abstract

Transcription of the Rhodobacter sphaeroides cytochrome c2 gene (cycA) is negatively regulated by both the presence of oxygen and intermediates in tetrapyrrole biosynthesis. A mutation responsible for uncoupling cycA transcription from tetrapyrrole availability was localized to a gene (chrR) that encodes a 357-amino-acid protein. Analysis of a defined chrR null mutation indicated that this protein positively regulated cycA transcription. From this and other results, it appeared that the positive action of ChrR on cycA transcription is blocked by altering the availability of either heme or some intermediate in tetrapyrrole biosynthesis. A single missense mutation which substitutes an Arg for a Cys at residue 182 of ChrR (C182R) was shown to be necessary and sufficient for the increased cycA transcription seen in the mutant strain Chr4. Thus, it appears that this C182R substitution generated an altered-function form of ChrR. In addition, by analyzing cycA transcription in delta ChrR strains, we showed that ChrR was not required for increased cycA transcription under anaerobic conditions. Instead, our results indicated that ChrR and the response regulator PrrA (J. M. Eraso and S. Kaplan, J. Bacteriol. 176:32-43, 1994) functioned independently at the upstream cycA promoter that is activated under anaerobic conditions.

摘要

球形红杆菌细胞色素c2基因(cycA)的转录受到氧的存在和四吡咯生物合成中间体的负调控。一个导致cycA转录与四吡咯可用性解偶联的突变定位于一个编码357个氨基酸蛋白质的基因(chrR)。对一个明确的chrR缺失突变的分析表明,该蛋白质正向调控cycA转录。基于此及其他结果,似乎ChrR对cycA转录的正向作用可通过改变血红素或四吡咯生物合成中某些中间体的可用性来阻断。在突变菌株Chr4中观察到cycA转录增加,结果表明,在ChrR的第182位残基处将一个半胱氨酸替换为精氨酸的单个错义突变(C182R)是必需且充分的。因此,似乎这种C182R替换产生了一种功能改变的ChrR形式。此外,通过分析缺失ChrR菌株中的cycA转录,我们发现厌氧条件下cycA转录增加并不需要ChrR。相反,我们的结果表明,ChrR与应答调节因子PrrA(J. M. Eraso和S. Kaplan,《细菌学杂志》176:32 - 43,1994)在厌氧条件下被激活的上游cycA启动子处独立发挥作用。

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