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大肠杆菌K-12厌氧诱导的nirB+基因缺乏氧化还原调控。

Lack of redox control of the anaerobically-induced nirB+ gene of Escherichia coli K-12.

作者信息

Griffiths L, Cole J A

出版信息

Arch Microbiol. 1987 May;147(4):364-9. doi: 10.1007/BF00406134.

Abstract

Operon fusion strains of Escherichia coli K-12 have been used to demonstrate that transcription of the structural gene for NADH-dependent nitrite reductase is regulated by oxygen repression and induction by its substrate, nitrite. This two-stage regulation of nirB is totally dependent upon a functional Fnr protein. Unlike the Fnr-dependent fumarate reductase operon, nirB transcription is not repressed by nitrate. These results suggest that the Fnr protein is simply a positive control protein essential for the derepression of some, but not all, anaerobically-induced operons rather than a more general redox-sensitive regulator, as suggested by the redox control hypothesis for the regulation of gene expression in facultatively anaerobic bacteria.

摘要

大肠杆菌K-12的操纵子融合菌株已被用于证明,依赖NADH的亚硝酸还原酶结构基因的转录受氧抑制调控,并受其底物亚硝酸盐的诱导。nirB的这种两阶段调控完全依赖于功能性的Fnr蛋白。与依赖Fnr的延胡索酸还原酶操纵子不同,nirB转录不受硝酸盐抑制。这些结果表明,Fnr蛋白只是一种正调控蛋白,对于一些(而非全部)厌氧诱导操纵子的去阻遏是必需的,而不是像兼性厌氧细菌基因表达调控的氧化还原控制假说所暗示的那样,是一种更普遍的氧化还原敏感调节因子。

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