The nitric oxide (NO)-Sensing repressor NsrR of Neisseria meningitidis has a compact regulon of genes involved in NO synthesis and detoxification
The nitric oxide (NO)-Sensing repressor NsrR of Neisseria meningitidis has a compact regulon of genes involved in NO synthesis and detoxification
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DOI：
10.1128/jb.01869-07
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发表时间：
2008-04-01
影响因子：
3.2
通讯作者：
Moir, James W. B.
中科院分区：
文献类型：
--
作者：
Heurlier, Karin;Thomson, Melanie J.;Moir, James W. B.
我们已经分析了一氧化氮（NO）敏感的阻遏物NsrR从脑膜炎奈瑟氏球菌MC58的调节程度，使用微阵列分析。基于NsrR突变体和野生型菌株之间的比较，通过定量实时PCR进一步研究了似乎受NsrR调控的靶基因，揭示了一组非常紧凑的基因，如下所示：诺布（编码NO还原酶），dnrN（编码一种参与修复铁硫簇亚硝化损伤的蛋白质pu13），aniA（编码亚硝酸还原酶）、nirV（推定的亚硝酸还原酶组装蛋白）和mobA（在其他物种中与钼代谢相关但在N.脑膜炎）。在所有情况下，NsrR都起着阻遏物的作用。NO保护系统norB和dnrN受NO的调控，且受NsrR的依赖，而NO保护系统细胞色素c'（cycP编码）则不受NO或NsrR的调控，表明N.脑膜炎表达组成型和诱导型NO保护系统。此外，我们提出的证据表明，厌氧反应调节剂FNR也对NO敏感，但不如NsrR敏感，导致启动子如aniA的复杂调节，这是由FNR和NsrR控制的：发现aniA最大程度地由中间NO浓度诱导，与允许在反硝化（其中NO积累）期间表达但当NO接近毒性浓度时下调的调节系统一致。
We have analyzed the extent of regulation by the nitric oxide (NO)-sensitive repressor NsrR from Neisseria meningitidis MC58, using microarray analysis. Target genes that appeared to be regulated by NsrR, based on a comparison between an nsrR mutant and a wild-type strain, were further investigated by quantitative real-time PCR, revealing a very compact set of genes, as follows: norB (encoding NO reductase), dnrN (encoding a protein putatively involved in the repair of nitrosative damage to iron-sulfur clusters), aniA (encoding nitrite reductase), nirV (a putative nitrite reductase assembly protein), and mobA (a gene associated with molybdenum metabolism in other species but with a frame shift in N. meningitidis). In all cases, NsrR acts as a repressor. The NO protection systems norB and dnrN are regulated by NO in an NsrR-dependent manner, whereas the NO protection system cytochrome c' (encoded by cycP) is not controlled by NO or NsrR, indicating that N. meningitidis expresses both constitutive and inducible NO protection systems. In addition, we present evidence to show that the anaerobic response regulator FNR is also sensitive to NO but less so than NsrR, resulting in complex regulation of promoters such as aniA, which is controlled by both FNR and NsrR: aniA was found to be maximally induced by intermediate NO concentrations, consistent with a regulatory system that allows expression during denitrification (in which NO accumulates) but is down-regulated as NO approaches toxic concentrations.