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铜绿假单胞菌中的双群体感应系统控制着铜绿假单胞菌喹诺酮信号(PQS)的产生。

Dueling quorum sensing systems in Pseudomonas aeruginosa control the production of the Pseudomonas quinolone signal (PQS).

作者信息

McGrath Stephen, Wade Dana S, Pesci Everett C

机构信息

Department of Microbiology and Immunology, The Brody School of Medicine, East Carolina University, Greenville, NC 27858, USA.

出版信息

FEMS Microbiol Lett. 2004 Jan 15;230(1):27-34. doi: 10.1016/S0378-1097(03)00849-8.

DOI:10.1016/S0378-1097(03)00849-8
PMID:14734162
Abstract

The opportunistic human pathogen Pseudomonas aeruginosa regulates the production of numerous virulence factors via the action of two separate but coordinated quorum sensing systems, las and rhl. These systems control the transcription of genes in response to population density through the intercellular signals N-(3-oxododecanoyl)-L-homoserine lactone (3-oxo-C(12)-HSL) and N-(butanoyl)-L-homoserine lactone (C(4)-HSL). A third P. aeruginosa signal, 2-heptyl-3-hydroxy-4-quinolone [Pseudomonas quinolone signal (PQS)], also plays a significant role in the transcription of multiple P. aeruginosa virulence genes. PQS is intertwined in the P. aeruginosa quorum sensing hierarchy with its production and bioactivity requiring the las and rhl quorum sensing systems, respectively. This report presents a preliminary transcriptional analysis of pqsA, the first gene of the recently discovered PQS biosynthetic gene cluster. We show that pqsA transcription required pqsR, a transcriptional activator protein encoded within the PQS biosynthetic gene cluster. It was also found that the transcription of pqsA and subsequent production of PQS was induced by the las quorum sensing system and repressed by the rhl quorum sensing system. In addition, PQS production was dependent on the ratio of 3-oxo-C(12)-HSL to C(4)-HSL, suggesting a regulatory balance between quorum sensing systems. These data are an important early step toward understanding the regulation of PQS synthesis and the role of PQS in P. aeruginosa intercellular signaling.

摘要

机会性人类病原体铜绿假单胞菌通过两个独立但相互协调的群体感应系统las和rhl的作用来调节多种毒力因子的产生。这些系统通过细胞间信号N-(3-氧代十二烷酰基)-L-高丝氨酸内酯(3-氧代-C(12)-HSL)和N-(丁酰基)-L-高丝氨酸内酯(C(4)-HSL)来控制基因转录以响应群体密度。铜绿假单胞菌的第三种信号2-庚基-3-羟基-4-喹诺酮[假单胞菌喹诺酮信号(PQS)]在多种铜绿假单胞菌毒力基因的转录中也起着重要作用。PQS在铜绿假单胞菌群体感应层级中相互交织,其产生和生物活性分别需要las和rhl群体感应系统。本报告对最近发现的PQS生物合成基因簇的第一个基因pqsA进行了初步转录分析。我们表明pqsA转录需要pqsR,pqsR是一种在PQS生物合成基因簇中编码的转录激活蛋白。还发现pqsA的转录以及随后PQS的产生受las群体感应系统诱导,并受rhl群体感应系统抑制。此外,PQS的产生取决于3-氧代-C(12)-HSL与C(4)-HSL的比例,这表明群体感应系统之间存在调节平衡。这些数据是朝着理解PQS合成调控以及PQS在铜绿假单胞菌细胞间信号传导中的作用迈出的重要早期步骤。

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