PnpM, a LysR-Type Transcriptional Regulator Activates the Hydroquinone Pathway in para-Nitrophenol Degradation in Pseudomonas sp. Strain WBC-3.
PnpM, a LysR-Type Transcriptional Regulator Activates the Hydroquinone Pathway in para-Nitrophenol Degradation in Pseudomonas sp. Strain WBC-3.
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PnpM 是一种 LysR 型转录调节剂，可激活假单胞菌 WBC-3 菌株对硝基苯酚降解中的对苯二酚途径
DOI：
10.3389/fmicb.2017.01714
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发表时间：
2017
影响因子：
5.2
通讯作者：
Zhou NY
中科院分区：
文献类型：
--
作者：
Wang JP;Zhang WM;Chao HJ;Zhou NY
LysR型转录调节因子（LTTR）PnpR先前已显示激活操纵子pnpA、pnpB和pnpCDEFG的转录，用于假单胞菌属菌株WBC-3中的对硝基苯酚（PNP）降解。进一步的初步证据表明，在pnpCDEFG的启动子区域中可能存在LTTR额外的结合位点。在这项研究中，一个额外的LTTR PnpM，它显示44%的同源性PnpR，被确定为激活pnpCDEFG的表达。有趣的是，pnpM缺失的WBC-3菌株不能在PNP上生长，但积累氢醌（HQ），其是PnpAB降解PNP的分解代谢产物和PnpCD的底物。通过电泳迁移率变动分析（EMSAs）和启动子活性检测，发现只有PnpR参与pnpA和pnpB的激活，而PnpR和PnpM均参与pnpCDEFG的激活。DNA酶I足迹分析表明，PnpR和PnpM在pnpCDEFG启动子中共享27 bp的DNA结合区。在PNP存在下，PnpR的保护区增加到39 bp，PnpM的保护区增加到38 bp。我们的数据表明，PnpR和PnpM都参与激活pnpCDEFG的表达，其中PNP而不是PnpCD的底物氢醌是诱导剂。因此，在假单胞菌菌株WBC-3的PNP催化过程中，用于最初两个反应的pnpA和pnpB操纵子由PnpR控制，而用于HQ降解的第三个操纵子（pnpCDEFG）由PnpM和PnpR激活。这项研究建立在我们以前的研究结果，并表明，两个LTTRs PnpR和PnpM参与这三个分解代谢操纵子的转录激活。具体而言，我们的鉴定，LTTR，PnpM，调节pnpCDEFG表达提供了新的见解，在一个有趣的PNP categories的调节系统，由两个监管机构控制。
A LysR-type transcriptional regulator (LTTR), PnpR, has previously been shown to activate the transcription of operons pnpA, pnpB, and pnpCDEFG for para-nitrophenol (PNP) degradation in Pseudomonas sp. strain WBC-3. Further preliminary evidence suggested the possible presence of an LTTR additional binding site in the promoter region of pnpCDEFG. In this study, an additional LTTR PnpM, which shows 44% homology to PnpR, was determined to activate the expression of pnpCDEFG. Interestingly, a pnpM-deleted WBC-3 strain was unable to grow on PNP but accumulating hydroquinone (HQ), which is the catabolic product from PNP degradation by PnpAB and the substrate for PnpCD. Through electrophoretic mobility shift assays (EMSAs) and promoter activity detection, only PnpR was involved in the activation of pnpA and pnpB, but both PnpR and PnpM were involved in the activation of pnpCDEFG. DNase I footprinting analysis suggested that PnpR and PnpM shared the same DNA-binding regions of 27 bp in the pnpCDEFG promoter. In the presence of PNP, the protection region increased to 39 bp by PnpR and to 38 bp by PnpM. Our data suggested that both PnpR and PnpM were involved in activating pnpCDEFG expression, in which PNP rather than the substrate hydroquinone for PnpCD is the inducer. Thus, during the PNP catabolism in Pseudomonas sp. strain WBC-3, pnpA and pnpB operons for the initial two reactions were controlled by PnpR, while the third operon (pnpCDEFG) for HQ degradation was activated by PnpM and PnpR. This study builds upon our previous findings and shows that two LTTRs PnpR and PnpM are involved in the transcriptional activation of these three catabolic operons. Specifically, our identification that an LTTR, PnpM, regulates pnpCDEFG expression provides new insights in an intriguing regulation system of PNP catabolism that is controlled by two regulators.