Transcriptional regulation of nitric oxide reduction in Ralstonia eutropha H16
Transcriptional regulation of nitric oxide reduction in Ralstonia eutropha H16
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DOI：
10.1042/bst0330193
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发表时间：
2005-02-01
影响因子：
3.9
通讯作者：
Cramm, R
中科院分区：
文献类型：
--
作者：
Büsch, A;Strube, K;Cramm, R
富营养菌H16的一氧化氮还原是由依赖于喹酚的NO还原酶Norb催化的。Norb和相邻的Nora形成一个操纵子，该操纵子受依赖于sigma(54)的转录激活子Norr控制，以响应NO。含有MERE而不是N-末端结构域的NorR衍生物与NorA上游73bp的区域结合，该区域包括推测的上游激活序列GGT-(N-7)-ACC的三个副本。改变该序列的个别碱基的突变导致野生型NorR转录激活减少80%-90%。在编码NO代谢蛋白的基因上游的几个蛋白细菌中也存在类似的基序。NorR的N-末端结构域包含一个GAF模块，并被假设与信号分子相互作用。缺少该结构域的NorR衍生物可结构性地激活norAB启动子。GAF模块内的氨基酸交换确定了半胱氨酸残基，这是NorR激活启动子所必需的。NorR的信号感应受到含铁蛋白NorA的负调节。
Nitric oxide reduction in Ralstonia eutropho H16 is catalysed by the quinol-dependent NO reductase NorB. norB and the adjacent norA form an operon that is controlled by the sigma(54)-dependent transcriptional activator NorR in response to NO. A NorR derivative containing MalE in place of the N-terminal domain binds to a 73 bp region upstream of norA that includes three copies of the putative upstream activator sequence GGT-(N-7)-ACC. Mutations altering individual bases of this sequence resulted in an 80-90% decrease in transcriptional activation by wild-type NorR. Similar motifs are present in several proteolbacteria upstream of genes encoding proteins of NO metabolism. The N-terminal domain of NorR contains a GAF module and is hypothesized to interact with a signal molecule. A NorR derivative lacking this domain activates the norAB promoter constitutively. Amino acid exchanges within the GAF module identified a cysteine residue that is essential for promoter activation by NorR. Signal sensing by NorR is negatively modulated by the iron-containing protein NorA.