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在假单胞菌属M18中,全局调控因子GacA、RsmA、LasI和RhlI对PltR表达的调控

PltR expression modulated by the global regulators GacA, RsmA, LasI and RhlI in Pseudomonas sp. M18.

作者信息

Huang Xianqing, Zhang Xuehong, Xu Yuquan

机构信息

Key Laboratory of Microbial Metabolism, Ministry of Education, College of Life Sciences and Biotechnology, Shanghai Jiao tong University, 800 Dongchuan Road, Shanghai 200240, PR China.

出版信息

Res Microbiol. 2008 Mar;159(2):128-36. doi: 10.1016/j.resmic.2007.10.006. Epub 2007 Nov 28.

DOI:10.1016/j.resmic.2007.10.006
PMID:18248796
Abstract

Pseudomonas sp. M18 can suppress certain soil-borne phytopathogenic fungi by producing two antibiotics, pyoluteorin (Plt) and phenazine-1-carboxylic acid (PCA). pltR encodes an LysR-type transcriptional activator required for expression of divergently transcribed Plt biosynthetic genes. Here we provide evidence that Plt biosynthesis is negatively regulated by the quorum-sensing (QS) signal molecule (N-acyl homoserine lactone, AHL) synthase gene lasI and positively regulated by the orphan LuxR-type regulatory gene vqsR. pltR expression is modulated by four important global regulators including the two-component response regulatory gene gacA, the RNA-binding repressor RsmA, and the QS signal molecule synthase genes lasI and rhlI. pltR translation was almost completely inhibited in the gacA mutant M18G when compared with that in the wild-type strain of M18. We also observed significant enhancement of pltR translation in the rsmA mutant compared with wild-type strain M18. Moreover, mutation in lasI or rhlI gave rise to a significantly elevated level of pltR transcription in strain M18. However, no obvious difference was observed in pltR expression between the vqsR mutant and the wild-type of strain M18. These results highlight the fact that PltR likely at least partly plays an important mediator role in Gac/Rsm and the Las/Rhl regulatory pathways involved in Plt biosynthesis.

摘要

铜绿假单胞菌M18能够通过产生两种抗生素——藤黄绿菌素(Plt)和吩嗪-1-羧酸(PCA)来抑制某些土传植物病原真菌。pltR编码一个LysR型转录激活因子,它是反向转录的Plt生物合成基因表达所必需的。在此,我们提供证据表明,Plt生物合成受到群体感应(QS)信号分子(N-酰基高丝氨酸内酯,AHL)合成酶基因lasI的负调控,并受到孤儿LuxR型调控基因vqsR的正调控。pltR的表达受到四个重要的全局调控因子的调节,包括双组分应答调控基因gacA、RNA结合阻遏物RsmA以及QS信号分子合成酶基因lasI和rhlI。与野生型M18菌株相比,在gacA突变体M18G中,pltR的翻译几乎完全受到抑制。我们还观察到,与野生型M18菌株相比,rsmA突变体中pltR的翻译显著增强。此外,lasI或rhlI的突变导致M18菌株中pltR的转录水平显著升高。然而,在vqsR突变体和M18菌株的野生型之间,未观察到pltR表达有明显差异。这些结果突出了这样一个事实,即PltR可能至少部分地在参与Plt生物合成的Gac/Rsm和Las/Rhl调控途径中发挥重要的介导作用。

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