INTERACTION OF 6 GLOBAL TRANSCRIPTION REGULATORS IN EXPRESSION OF MANGANESE SUPEROXIDE-DISMUTASE IN ESCHERICHIA-COLI K-12

INTERACTION OF 6 GLOBAL TRANSCRIPTION REGULATORS IN EXPRESSION OF MANGANESE SUPEROXIDE-DISMUTASE IN ESCHERICHIA-COLI K-12
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DOI:
10.1128/jb.175.6.1687-1696.1993
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发表时间:
1993-03-01
影响因子:
3.2
通讯作者:
TOUATI, D
TOUATI, D
中科院分区:
生物学3区
文献类型:
--
作者:
COMPAN, I;TOUATI, D

文献摘要

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编码锰超氧化物歧化酶的大肠杆菌 sodA 基因的转录受到六个全局调节因子的控制:soxRS 基因座(超氧化物反应)和 soxQ 基因座突变等位基因(例如 cfxB)的产物充当激活剂; Fur(铁摄取调节)、arcA(有氧调节控制)和 fnr(富马酸硝酸还原酶)基因以及整合宿主因子 (IHF) 的产物对 sodA 进行负调节。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效应基因中携带不同无效突变组合的菌株,研究了这些效应子对 sodA 启动子的作用。这些数据使我们能够指定 sodA 启动子中的目标区域,以便由 SoxRS 和 CfxB 激活,并由 Fur 和 ArcA 抑制。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 对照是相互排斥的。 Fnr 的镇压似乎至少部分依赖于 ArcA。 IHF 增强了有氧 Fur 抑制,而在没有 Fur 的情况下,它增强了 ArcA 的无氧抑制。 Fur(包含 -35 区域)和 ArcA(来自 -35 区域及其下游)的 DNA 靶标似乎重叠,表明 Fur 和 ArcA 抑制是相互排斥的。 Fur(响应铁池)或 ArcA 与 Fnr 和 IHF(响应细胞的氧化还原状态)一起作用,可以以大约相同的效率阻断厌氧 sodA-lacZ 表达。讨论了该结果可能的生物学意义。
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.