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MtrA是MtrAB双组分系统的一个必需应答调节因子,可调控结核分枝杆菌复苏促进因子B的转录。

MtrA, an essential response regulator of the MtrAB two-component system, regulates the transcription of resuscitation-promoting factor B of Mycobacterium tuberculosis.

作者信息

Sharma Arun Kumar, Chatterjee Ayan, Gupta Shamba, Banerjee Rajdeep, Mandal Sukhendu, Mukhopadhyay Jayanta, Basu Joyoti, Kundu Manikuntala

机构信息

1Department of Chemistry, Bose Institute, 93/1 Acharya Prafulla Chandra Road, Kolkata 700009, India.

2Department of Biochemistry, Bose Institute, P-1/12 CIT Scheme VII M, Kolkata 700054, India.

出版信息

Microbiology (Reading). 2015 Jun;161(6):1271-81. doi: 10.1099/mic.0.000087. Epub 2015 Apr 1.

Abstract

The resuscitation-promoting factors of Mycobacterium tuberculosis are hydrolytic enzymes, which are required for resuscitation of dormant cells. RpfB, a peptidoglycan remodelling enzyme similar to the lytic transglycosylase of Escherichia coli, is required for reactivation of M. tuberculosis from chronic infection in vivo, underscoring the need to understand its transcriptional regulation. Here, we identified the transcriptional and translational start points of rpfB, and suggested from rpf promoter-driven GFP expression and in vitro transcription assays that its transcription possibly occurs in a SigB-dependent manner. We further demonstrated that rpfB transcription is regulated by MtrA - the response regulator of the essential two-component system MtrAB. Association of MtrA with the rpfB promoter region in vivo was confirmed by chromatin immunoprecipitation analysis. Electrophoretic mobility shift assays (EMSAs) revealed a loose direct repeat sequence associated with MtrA binding. Binding of MtrA was enhanced upon phosphorylation. MtrA could be pulled down from lysates of M. tuberculosis using a biotinylated DNA fragment encompassing the MtrA-binding site on the rpfB promoter, confirming that MtrA binds to the rpfB promoter. Enhanced GFP fluorescence driven by the rpfB promoter, upon deletion of the MtrA-binding site, and repression of rpfB expression, upon overexpression of MtrA, suggested that MtrA functions as a repressor of rpfB transcription. This was corroborated by EMSAs showing diminished association of RNA polymerase (RNAP) with the rpfB promoter in the presence of MtrA. In vitro transcription assays confirmed that MtrA inhibits RNAP-driven rpfB transcription.

摘要

结核分枝杆菌的复苏促进因子是水解酶,它们是休眠细胞复苏所必需的。RpfB是一种与大肠杆菌溶菌转糖基酶类似的肽聚糖重塑酶,是体内慢性感染的结核分枝杆菌重新激活所必需的,这突出了了解其转录调控的必要性。在这里,我们确定了rpfB的转录和翻译起始点,并通过rpf启动子驱动的绿色荧光蛋白(GFP)表达和体外转录试验表明,其转录可能以依赖SigB的方式发生。我们进一步证明,rpfB转录受MtrA调控——MtrAB必需双组分系统的应答调节因子。通过染色质免疫沉淀分析证实了MtrA在体内与rpfB启动子区域的结合。电泳迁移率变动分析(EMSA)揭示了一个与MtrA结合相关的松散直接重复序列。MtrA磷酸化后结合增强。使用包含rpfB启动子上MtrA结合位点的生物素化DNA片段,可以从结核分枝杆菌裂解物中拉下MtrA,证实MtrA与rpfB启动子结合。删除MtrA结合位点后,rpfB启动子驱动的GFP荧光增强,而MtrA过表达时,rpfB表达受到抑制,这表明MtrA作为rpfB转录的抑制因子发挥作用。EMSA显示在有MtrA存在时RNA聚合酶(RNAP)与rpfB启动子的结合减少,这证实了这一点。体外转录试验证实MtrA抑制RNAP驱动的rpfB转录。

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