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The Signal Transduction Protein GlnK Is Required for NifL-Dependent Nitrogen Control of nif Gene Expression in Klebsiella pneumoniae

机译:信号转导蛋白GlnK是肺炎克雷伯菌中nif基因表达的NifL依赖型氮控制所必需的

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摘要

In Klebsiella pneumoniae, transcription of the nitrogen fixation (nif) genes is regulated in response to molecular oxygen or availability of fixed nitrogen by the coordinated activities of the nifA and nifL gene products. NifA is a nif-specific transcriptional activator, the activity of which is inhibited by interaction with NifL. Nitrogen control of NifL occurs at two levels: transcription of the nifLA operon is regulated by the global ntr system, and the inhibitory activity of NifL is controlled in response to fixed nitrogen by an unknown factor. K. pneumoniae synthesizes two PII-like signal transduction proteins, GlnB, which we have previously shown not to be involved in the response of NifL to fixed nitrogen, and the recently identified protein GlnK. We have now cloned the K. pneumoniae glnK gene, studied its expression, and shown that a null mutation in glnK prevents NifL from responding to the absence of fixed nitrogen, i.e., from relieving the inhibition of NifA activity. Hence, GlnK appears to be involved, directly or indirectly, in NifL-dependent regulation of nif gene expression in K. pneumoniae. Comparison of the GlnB and GlnK amino acid sequences from six species of proteobacteria identifies five residues (residues 3, 5, 52, 54, and 64) which serve to distinguish the GlnB and GlnK proteins.
机译:在肺炎克雷伯氏菌中,固氮(nif)基因的转录是通过nifA和nifL基因产物的协调活性来响应分子氧或固定氮的可用性而调节的。 NifA是nif特异性转录激活因子,其活性受与NifL相互作用的抑制。 NifL的氮控制分为两个级别:nifLA操纵子的转录受全局ntr系统调控,而NifL的抑制活性由未知因素响应固定氮而控制。肺炎克雷伯氏菌合成两种PII样信号转导蛋白GlnB,我们先前已证明它们不参与NifL对固定氮的应答,以及最近鉴定出的蛋白GlnK。现在我们已经克隆了肺炎克雷伯氏菌glnK基因,研究了其表达,并显示glnK中的无效突变可阻止NifL对固定氮的缺乏做出反应,即减轻对NifA活性的抑制。因此,GlnK似乎直接或间接参与了肺炎克雷伯菌中nifL基因表达的NifL依赖性调控。比较来自六种变形杆菌的GlnB和GlnK氨基酸序列,可鉴定出五个残基(残基3、5、52、54和64),这些残基用于区分GlnB和GlnK蛋白。

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