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铜绿假单胞菌细胞外喹诺酮信号传导所需的功能。

Functions required for extracellular quinolone signaling by Pseudomonas aeruginosa.

作者信息

Gallagher Larry A, McKnight Susan L, Kuznetsova Marina S, Pesci Everett C, Manoil Colin

机构信息

Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA.

出版信息

J Bacteriol. 2002 Dec;184(23):6472-80. doi: 10.1128/JB.184.23.6472-6480.2002.

DOI:10.1128/JB.184.23.6472-6480.2002
PMID:12426334
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC135424/
Abstract

A set of 30 mutants exhibiting reduced production of the phenazine poison pyocyanin were isolated following transposon mutagenesis of Pseudomonas aeruginosa PAO1. The mutants could be subdivided into those with defects in the primary phenazine biosynthetic pathway and those with more pleiotropic defects. The largest set of pleiotropic mutations blocked the production of the extracellular Pseudomonas quinolone signal (PQS), a molecule required for the synthesis of secondary metabolites and extracellular enzymes. Most of these pqs mutations affected genes which appear to encode PQS biosynthetic functions, although a transcriptional regulator and an apparent response effector were also represented. Two of the genes required for PQS synthesis (phnA and phnB) had previously been assumed to encode phenazine biosynthetic functions. The transcription of one of the genes required for PQS synthesis (PA2587/pqsH) was regulated by the LasI/R quorum-sensing system, thereby linking quorum sensing and PQS regulation. Others of the pleiotropic phenazine-minus mutations appear to inactivate novel components of the quorum-sensing regulatory network, including one regulator (np20) previously shown to be required for virulence in neutropenic mice.

摘要

在对铜绿假单胞菌PAO1进行转座子诱变后,分离出了一组30个突变体,这些突变体产生吩嗪毒素绿脓菌素的量减少。这些突变体可分为初级吩嗪生物合成途径有缺陷的突变体和具有更多多效性缺陷的突变体。最大的一组多效性突变阻断了细胞外铜绿假单胞菌喹诺酮信号(PQS)的产生,PQS是一种合成次级代谢产物和细胞外酶所需的分子。这些pqs突变中的大多数影响了似乎编码PQS生物合成功能的基因,不过也有一个转录调节因子和一个明显的反应效应器。PQS合成所需的两个基因(phnA和phnB)以前被认为编码吩嗪生物合成功能。PQS合成所需的一个基因(PA2587/pqsH)的转录受LasI/R群体感应系统调控,从而将群体感应与PQS调节联系起来。其他多效性吩嗪缺陷突变似乎使群体感应调节网络的新组分失活,包括一个先前已证明在中性粒细胞减少小鼠中对毒力有要求的调节因子(np20)。

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