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大肠杆菌产生一氧化氮。依赖于亚硝酸还原酶、一氧化氮感应调节因子Fnr和黄素血红蛋白Hmp。

Nitric oxide formation by Escherichia coli. Dependence on nitrite reductase, the NO-sensing regulator Fnr, and flavohemoglobin Hmp.

作者信息

Corker Hazel, Poole Robert K

机构信息

Department of Molecular Biology and Biotechnology, The University of Sheffield, Firth Court, Western Bank, Sheffield S10 2TN, United Kingdom.

出版信息

J Biol Chem. 2003 Aug 22;278(34):31584-92. doi: 10.1074/jbc.M303282200. Epub 2003 Jun 3.

Abstract

Nitric oxide (NO) is a key signaling and defense molecule in biological systems. The bactericidal effects of NO produced, for example, by macrophages are resisted by various bacterial NO-detoxifying enzymes, the best understood being the flavohemoglobins exemplified by Escherichia coli Hmp. However, many bacteria, including E. coli, are reported to produce NO by processes that are independent of denitrification in which NO is an obligatory intermediate. We demonstrate using an NO-specific electrode that E. coli cells, grown anaerobically with nitrate as terminal electron acceptor, generate significant NO on adding nitrite. The periplasmic cytochrome c nitrite reductase (Nrf) is shown, by comparing Nrf+ and Nrf- mutants, to be largely responsible for NO generation. Surprisingly, an hmp mutant did not accumulate more NO but, rather, failed to produce detectable NO. Anaerobic growth of the hmp mutant was not stimulated by nitrate, and the mutant failed to produce periplasmic cytochrome(s) c, leading to the hypothesis that accumulating NO in the absence of Hmp inactivates the global anaerobic regulator Fnr by reaction with the [4Fe-4S]2+ cluster (Cruz-Ramos, H., Crack, J., Wu, G., Hughes, M. N., Scott, C., Thomson, A. J., Green, J., and Poole, R. K. (2002) EMBO J. 21, 3235-3244). Fnr thus failed to up-regulate nitrite reductase. The model is supported by the inability of an fnr mutant to generate NO and by the restoration of NO accumulation to hmp mutants upon introducing a plasmid encoding Fnr* (D154A) known to confer activity in the presence of oxygen. A cytochrome bd-deficient mutant retained NO-generating activity. The present study reveals a critical balance between NO-generating and -detoxifying activities during anaerobic growth.

摘要

一氧化氮(NO)是生物系统中的关键信号和防御分子。巨噬细胞产生的NO具有杀菌作用,但各种细菌的NO解毒酶可抵抗这种作用,其中最被熟知的是大肠杆菌Hmp所代表的黄素血红蛋白。然而,据报道,包括大肠杆菌在内的许多细菌通过独立于反硝化作用的过程产生NO,在反硝化作用中,NO是必不可少的中间产物。我们使用NO特异性电极证明,以硝酸盐作为末端电子受体进行厌氧培养的大肠杆菌细胞,在添加亚硝酸盐时会产生大量NO。通过比较Nrf +和Nrf-突变体表明,周质细胞色素c亚硝酸盐还原酶(Nrf)在很大程度上负责NO的产生。令人惊讶的是,hmp突变体并没有积累更多的NO,而是未能产生可检测到的NO。hmp突变体的厌氧生长不受硝酸盐的刺激,并且该突变体未能产生周质细胞色素c,这导致了一个假设,即在没有Hmp的情况下积累的NO通过与[4Fe-4S] 2+簇反应使全局厌氧调节因子Fnr失活(Cruz-Ramos,H.,Crack,J.,Wu,G.,Hughes,M.N.,Scott,C.,Thomson,A.J.,Green,J.和Poole,R.K.(2002)EMBO J. 21,3235 - 3244)。因此,Fnr未能上调亚硝酸盐还原酶。该模型得到了fnr突变体无法产生NO以及在引入编码Fnr *(D154A)的质粒后hmp突变体恢复NO积累的支持,已知该质粒在有氧条件下具有活性。细胞色素bd缺陷型突变体保留了产生NO的活性。本研究揭示了厌氧生长过程中NO产生和解毒活性之间的关键平衡。

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