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在 rpoS 突变的铜绿假单胞菌中,phz1 比 phz2 对吩嗪-1-羧酸生物合成的贡献更大。

phz1 contributes much more to phenazine-1-carboxylic acid biosynthesis than phz2 in Pseudomonas aeruginosa rpoS mutant.

机构信息

Department of Applied and Environmental Microbiology, School of Life Sciences, Ludong University, Yantai, China.

Laboratory of Applied and Environmental Microbiology, Institute of Applied Microbiology, Xinjiang Academy of Agricultural Sciences, Urumqi, China.

出版信息

J Basic Microbiol. 2019 Sep;59(9):914-923. doi: 10.1002/jobm.201900165. Epub 2019 Jul 11.

DOI:10.1002/jobm.201900165
PMID:31294863
Abstract

Pseudomonas aeruginosa PAO1, a common opportunistic bacterial pathogen, contains two phenazine-biosynthetic operons, phz1 (phzA B C D E F G ) and phz2 (phzA B C D E F G ). Each of two operons can independently encode a set of enzymes involving in the biosynthesis of phenazine-1-carboxylic acid. As a global transcriptional regulator, RpoS mediates a lot of genes involving secondary metabolites biosynthesis in many bacteria. In an other previous study, it was reported that RpoS deficiency caused overproduction of pyocyanin, a derivative of phenazine-1-carboxylic acid in P. aeruginosa PAO1. But it is not known how RpoS mediates the expression of each of two phz operons and modulates phenazine-1-carboxylic acid biosynthesis in detail. In this study, by deleting the rpoS gene in the mutant PNΔphz1 and the mutant PNΔphz2, we found that the phz1 operon contributes much more to phenazine-1-carboxylic acid biosynthesis than the phz2 operon in the absence of RpoS. With the construction of the translational and transcriptional fusion vectors with the truncated lacZ reporter gene, we demonstrated that RpoS negatively regulates the expression of phz1 and positively controls the expression of phz2, and the regulation of phenazine-1-carboxylic acid biosynthesis mediated by RopS occurs at the posttranscriptional level, not at the transcriptional level. Obviously, two copies of phz operons and their differential expression mediated by RpoS might help P. aeruginosa adapt to its diverse environments and establish infection in its hosts.

摘要

铜绿假单胞菌 PAO1 是一种常见的机会性细菌病原体,它包含两个吩嗪生物合成操纵子,phz1(phzA B C D E F G)和 phz2(phzA B C D E F G)。两个操纵子中的每一个都可以独立编码一组参与吩嗪-1-羧酸生物合成的酶。作为一种全局转录调节因子,RpoS 介导许多涉及许多细菌中次生代谢物生物合成的基因。在之前的一项研究中,据报道,RpoS 缺乏会导致铜绿假单胞菌 PAO1 中吩嗪-1-羧酸的衍生物绿脓菌素的过量产生。但目前尚不清楚 RpoS 如何调节两个 phz 操纵子的表达,并详细调节吩嗪-1-羧酸的生物合成。在这项研究中,通过在突变体 PNΔphz1 和突变体 PNΔphz2 中缺失 rpoS 基因,我们发现,在没有 RpoS 的情况下,phz1 操纵子对吩嗪-1-羧酸的生物合成的贡献比 phz2 操纵子大得多。通过构建带有截短的 lacZ 报告基因的转录和翻译融合载体,我们证明 RpoS 负调控 phz1 的表达,正调控 phz2 的表达,并且 RopS 介导的吩嗪-1-羧酸生物合成的调节发生在转录后水平,而不是转录水平。显然,两个 phz 操纵子及其拷贝数差异表达由 RpoS 介导,可能有助于铜绿假单胞菌适应其多样化的环境并在其宿主中建立感染。

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