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ArcA和Fnr参与大肠杆菌硫醇过氧化物酶基因的表达。

Involvement of ArcA and Fnr in expression of Escherichia coli thiol peroxidase gene.

作者信息

Kim S J, Han Y H, Kim I H, Kim H K

机构信息

Department of Genetic Engineering, Pai-Chai University Taejon, Republic of Korea.

出版信息

IUBMB Life. 1999 Aug;48(2):215-8. doi: 10.1080/713803496.

Abstract

To explore the oxygen response regulators involved in thiol peroxidase gene (tpx) expression in Escherichia coli, we constructed a single-copy tpx-lacZ operon fusion and monitored tpx-lacZ expression in various genetic backgrounds. Expression of the tpx-lacZ fusion was increased 4-fold by aerobic growth. Anaerobic expression of tpx-lacZ in either (delta)arcA or delta(fnr) strains was 2.5-fold depressed compared with that of the wild-type strain. The results of immunoblotting experiments also demonstrated that ArcA and Fnr regulatory proteins repressed thiol peroxidase gene expression during anaerobic growth. Inspection of the tpx promoter region revealed putative binding sites for ArcA and Fnr. It thus appears that ArcA and Fnr function as repressors by blocking the binding of RNA polymerase to the tpx promoter in E. coli under anaerobic growth conditions.

摘要

为了探究大肠杆菌中参与硫醇过氧化物酶基因(tpx)表达的氧反应调节因子,我们构建了一个单拷贝的tpx-lacZ操纵子融合体,并在各种遗传背景下监测tpx-lacZ的表达。有氧生长使tpx-lacZ融合体的表达增加了4倍。与野生型菌株相比,tpx-lacZ在(delta)arcA或delta(fnr)菌株中的厌氧表达降低了2.5倍。免疫印迹实验结果还表明,ArcA和Fnr调节蛋白在厌氧生长期间抑制硫醇过氧化物酶基因的表达。对tpx启动子区域的检查揭示了ArcA和Fnr的假定结合位点。因此,在厌氧生长条件下,ArcA和Fnr似乎通过阻止RNA聚合酶与大肠杆菌中tpx启动子的结合而作为阻遏物发挥作用。

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