LysR family transcriptional regulator PqsR as repressor of pyoluteorin biosynthesis and activator of phenazine-1-carboxylic acid biosynthesis in Pseudomonas sp M18
LysR family transcriptional regulator PqsR as repressor of pyoluteorin biosynthesis and activator of phenazine-1-carboxylic acid biosynthesis in Pseudomonas sp M18
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LysR 家族转录调节因子 PqsR 作为假单胞菌 M18 中脓毒素生物合成的阻遏物和吩嗪-1-羧酸生物合成的激活剂
DOI：
10.1016/j.jbiotec.2009.06.008
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发表时间：
2009-08-10
影响因子：
4.1
通讯作者：
Xu, Yuquan
中科院分区：
文献类型：
--
作者：
Lu, Jishun;Huang, Xianqing;Xu, Yuquan
生防根际细菌假单胞菌属M18能够产生两种不同类型的抗生素，藤黄绿菌素（Plt）和吩嗪 - 1 - 羧酸（PCA），它们对多种土传植物病原菌具有抑制作用。在假单胞菌属M18中鉴定出的pqsR基因，在假单胞菌喹诺酮信号（PQS）介导的群体感应（QS）系统中编码一种LysR型转录调节因子。在此我们研究了PqsR在PCA和Plt生物合成中的调控机制。结果明确表明，PqsR作为一种双重功能的转录调节因子发挥作用，既是Plt生物合成的阻遏物，又是PCA生物合成的激活剂。pqsR基因的染色体失活导致Plt产量及其基因表达显著增强，而PCA产量及其基因表达几乎完全被抑制。这通过多个pqsR基因剂量实验、lacZ融合报告基因分析以及半定量逆转录聚合酶链反应（RT - PCR）得到了进一步证实。此外，PqsR对Plt途径特异性激活因子PltR的表达影响很小，这表明PqsR不是通过中介因子PltR对Plt生物合成施加负调控。另外，pqsR突变对负责合成N - 酰基高丝氨酸内酯（C4和C8 - HSLs）的RhlI的产生没有任何明显影响。这一结果表明，PqsR作为一种关键的转录调节因子独立于rhl QS系统发挥作用。（C）2009爱思唯尔有限公司。保留所有权利。
The biocontrol rhizobacterium Pseudomonas sp. M18 can produce two different types of antibiotics, pyoluteorin (Plt)and phenazine-1-carboxylic acid (PCA), which are inhibitory to a number of soil-borne plant pathogens. The pqsR gene, identified in Pseudomonas sp. M18, encodes a LysR-type transcriptional regulator in the Pseudomonas quinolone signal (PQS)-mediated quorum-sensing (QS) system. Here we investigated the regulatory mechanisms of PqsR in PCA and Plt biosyntheses. The results clearly suggest that PqsR functions as a double-duty transcriptional regulator, either as a repressor of Plt biosynthesis or as an activator of PCA biosynthesis. The chromosomal inactivation of pqsR resulted in significant enhancement of Pit production and its genes expression, while almost full inhibition of PCA production and its genes expression. This was further confirmed by multiple pqsR gene dosage experiments, lacZ fusion reporter analysis, and semi-quantitative RT-PCR. Furthermore, PqsR had little effect on expression of the pit pathway-specific activator PltR, indicating that PqsR does not exert its negative regulation on Plt biosynthesis through the mediator PltR. In addition, the pqsR mutation did not have any obvious influence on production of RhlI directing N-acylhomoserine lactones (C4 and C8-HSLs). This result shows PqsR functions as a crucial transcriptional regulator independently of the rill QS system. (C) 2009 Elsevier B.V. All rights reserved.