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Systematic analysis of diguanylate cyclases that promote biofilm formation by Pseudomonas fluorescens Pf0-1.系统分析促进荧光假单胞菌 Pf0-1 生物膜形成的双鸟苷酸环化酶。
J Bacteriol. 2011 Sep;193(18):4685-98. doi: 10.1128/JB.05483-11. Epub 2011 Jul 15.
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Phenazine-1-carboxylic acid promotes bacterial biofilm development via ferrous iron acquisition.吩嗪-1-羧酸通过获取二价铁促进细菌生物膜的形成。
J Bacteriol. 2011 Jul;193(14):3606-17. doi: 10.1128/JB.00396-11. Epub 2011 May 20.
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Modulation of Pseudomonas aeruginosa surface-associated group behaviors by individual amino acids through c-di-GMP signaling.通过 c-di-GMP 信号转导调节铜绿假单胞菌表面相关群体行为的个体氨基酸。
Res Microbiol. 2011 Sep;162(7):680-8. doi: 10.1016/j.resmic.2011.04.014. Epub 2011 Apr 30.
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The Pseudomonas quinolone signal (PQS), and its precursor HHQ, modulate interspecies and interkingdom behaviour.铜绿假单胞菌喹诺酮信号(PQS)及其前体 HHQ 调节种间和种间行为。
FEMS Microbiol Ecol. 2011 Aug;77(2):413-28. doi: 10.1111/j.1574-6941.2011.01121.x. Epub 2011 May 26.
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Specific control of Pseudomonas aeruginosa surface-associated behaviors by two c-di-GMP diguanylate cyclases.两种 c-di-GMP 二鸟苷酸环化酶特异性控制铜绿假单胞菌表面相关行为。
mBio. 2010 Oct 19;1(4):e00183-10. doi: 10.1128/mBio.00183-10.
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4-Quinolones: smart phones of the microbial world.4-喹诺酮类:微生物世界的智能手机。
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Oxygen levels rapidly modulate Pseudomonas aeruginosa social behaviours via substrate limitation of PqsH.氧气水平通过对 PqsH 的底物限制快速调节铜绿假单胞菌的社交行为。
Mol Microbiol. 2010 Sep;77(6):1527-38. doi: 10.1111/j.1365-2958.2010.07303.x. Epub 2010 Aug 17.
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Candida albicans-produced farnesol stimulates Pseudomonas quinolone signal production in LasR-defective Pseudomonas aeruginosa strains.白念珠菌产生的法呢醇可刺激 LasR 缺陷型铜绿假单胞菌菌株中绿脓菌素的信号产生。
Microbiology (Reading). 2010 Oct;156(Pt 10):3096-3107. doi: 10.1099/mic.0.037911-0. Epub 2010 Jul 23.
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Transcriptomic analysis reveals a global alkyl-quinolone-independent regulatory role for PqsE in facilitating the environmental adaptation of Pseudomonas aeruginosa to plant and animal hosts.转录组分析揭示了 PqsE 在促进铜绿假单胞菌适应植物和动物宿主方面的全局烷基-喹诺酮独立调控作用。
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2-庚基-4-喹诺酮,假单胞菌群体感应信号分子的前体,调节铜绿假单胞菌的群集运动。

2-Heptyl-4-quinolone, a precursor of the Pseudomonas quinolone signal molecule, modulates swarming motility in Pseudomonas aeruginosa.

机构信息

Department of Microbiology and Immunology, Dartmouth Medical School, Hanover, NH 03755, USA.

出版信息

J Bacteriol. 2011 Dec;193(23):6770-80. doi: 10.1128/JB.05929-11. Epub 2011 Sep 30.

DOI:10.1128/JB.05929-11
PMID:21965567
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3232867/
Abstract

Pseudomonas aeruginosa is an opportunistic pathogen capable of group behaviors, including biofilm formation and swarming motility. These group behaviors are regulated by both the intracellular signaling molecule c-di-GMP and acylhomoserine lactone quorum-sensing systems. Here, we show that the Pseudomonas quinolone signal (PQS) system also contributes to the regulation of swarming motility. Specifically, our data indicate that 2-heptyl-4-quinolone (HHQ), a precursor of PQS, likely induces the production of the phenazine-1-carboxylic acid (PCA), which in turn acts via an as-yet-unknown downstream mechanism to repress swarming motility. We show that this HHQ- and PCA-dependent swarming repression is apparently independent of changes in global levels of c-di-GMP, suggesting complex regulation of this group behavior.

摘要

铜绿假单胞菌是一种机会性病原体,能够进行群体行为,包括生物膜形成和群集运动。这些群体行为受到胞内信号分子 c-di-GMP 和酰基高丝氨酸内酯群体感应系统的调节。在这里,我们表明,铜绿假单胞菌喹诺酮信号(PQS)系统也有助于调节群集运动。具体而言,我们的数据表明,2-庚基-4-喹诺酮(HHQ),PQS 的前体,可能诱导吩嗪-1-羧酸(PCA)的产生,PCA 反过来通过一个尚未知的下游机制来抑制群集运动。我们表明,这种依赖于 HHQ 和 PCA 的群集抑制显然与 c-di-GMP 的全局水平变化无关,表明对这种群体行为的复杂调节。