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六种全局转录调节因子在大肠杆菌K-12中超氧化物歧化酶表达中的相互作用

Interaction of six global transcription regulators in expression of manganese superoxide dismutase in Escherichia coli K-12.

作者信息

Compan I, Touati D

机构信息

Institut Jacques Monod, Centre National de la Recherche Scientifique, Université Paris 7, France.

出版信息

J Bacteriol. 1993 Mar;175(6):1687-96. doi: 10.1128/jb.175.6.1687-1696.1993.

Abstract

Transcription of the sodA gene of Escherichia coli, which encodes manganese superoxide dismutase, is governed by six global regulators: the product of the soxRS locus (superoxide response) and mutated alleles of the soxQ locus (such as cfxB) act as activators; the products of the fur (ferric uptake regulation), arcA (aerobic regulation control), and fnr (fumarate nitrate reductase) genes and the integration host factor (IHF) negatively regulate sodA. The action of these effectors on the sodA promoter was investigated by using chromosomal sodA-lacZ operon fusions with intact or deleted promoters, different environmental conditions, and strains carrying different combinations of null mutations in the effector genes. The data allow us to assign target regions in the sodA promoter for activation by SoxRS and CfxB and for repression by Fur and ArcA. In aerobiosis, activation of sodA transcription by SoxRS was compatible with CfxB activation or Fur repression, whereas cfxB and fur controls were mutually exclusive. Repression by Fnr appeared, at least in part, to be ArcA dependent. IHF enhanced aerobic Fur repression, and in the absence of Fur, it enhanced anaerobic repression by ArcA. The DNA targets for Fur (encompassing the -35 region) and ArcA (from and downstream of the -35 region) appear to overlap, suggesting that Fur and ArcA repressions are mutually exclusive. Fur (in response to the iron pool) or ArcA, acting with Fnr and IHF (in response to the redox state of the cells), can block anaerobic sodA-lacZ expression with about equivalent efficiencies. The possible biological significance of this result is discussed.

摘要

大肠杆菌中编码锰超氧化物歧化酶的sodA基因的转录受六个全局调节因子控制:soxRS位点的产物(超氧化物应答)和soxQ位点的突变等位基因(如cfxB)起激活作用;fur(铁摄取调节)、arcA(需氧调节控制)和fnr(延胡索酸硝酸还原酶)基因的产物以及整合宿主因子(IHF)对sodA起负调节作用。通过使用具有完整或缺失启动子的染色体sodA-lacZ操纵子融合体、不同的环境条件以及在效应基因中携带不同组合无效突变的菌株,研究了这些效应因子对sodA启动子的作用。这些数据使我们能够确定sodA启动子中被SoxRS和CfxB激活以及被Fur和ArcA抑制的靶区域。在需氧条件下,SoxRS对sodA转录的激活与CfxB激活或Fur抑制相容,而cfxB和fur的控制相互排斥。Fnr的抑制作用至少部分依赖于ArcA。IHF增强了需氧条件下Fur的抑制作用,在没有Fur的情况下,它增强了ArcA的厌氧抑制作用。Fur(包含-35区域)和ArcA(-35区域及其下游)的DNA靶标似乎重叠,这表明Fur和ArcA的抑制作用相互排斥。Fur(响应铁池)或ArcA与Fnr和IHF(响应细胞的氧化还原状态)共同作用,可以以大致相同的效率阻断厌氧sodA-lacZ的表达。本文讨论了这一结果可能的生物学意义。

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