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铜绿假单胞菌的一种体内可诱导基因编码一种抗ExsA蛋白以抑制Ⅲ型分泌系统。

An in vivo inducible gene of Pseudomonas aeruginosa encodes an anti-ExsA to suppress the type III secretion system.

作者信息

Ha Un-Hwan, Kim Jaewha, Badrane Hassan, Jia Jinghua, Baker Henry V, Wu Donghai, Jin Shouguang

机构信息

Department of Molecular Genetics and Microbiology, PO Box 100266, University of Florida, Gainesville, FL 32610, USA.

出版信息

Mol Microbiol. 2004 Oct;54(2):307-20. doi: 10.1111/j.1365-2958.2004.04282.x.

DOI:10.1111/j.1365-2958.2004.04282.x
PMID:15469505
Abstract

We have previously reported on the isolation of in vivo inducible genes of Pseudomonas aeruginosa using IVET system. One of such genes isolated from burn mouse infection model encodes a short open reading frame with unknown function. In this study, we demonstrate that this gene product specifically suppresses the expression of type III secretion genes in P. aeruginosa, thus named PtrA (Pseudomonas type III repressor A). A direct interaction between the PtrA and type III transcriptional activator ExsA was demonstrated, suggesting that its repressor function is probably realized through inhibition of the ExsA protein function. Indeed, an elevated expression of the exsA compensates the repressor effect of the PtrA. Interestingly, expression of the ptrA is highly and specifically induced by copper cation. A copper- responsive two-component regulatory system, copR-copS, has also been identified and shown to be essential for the copper resistance in P. aeruginosa as well as the activation of ptrA in response to the copper signal. Elevated expression of the ptrA during the infection of mouse burn wound suggests that P. aeruginosa has evolved tight regulatory systems to shut down energy-expensive type III secretion apparatus in response to specific environmental signals, such as copper stress.

摘要

我们之前报道过使用体内表达技术(IVET)系统分离铜绿假单胞菌体内可诱导基因。从烧伤小鼠感染模型中分离出的此类基因之一编码一个功能未知的短开放阅读框。在本研究中,我们证明该基因产物特异性抑制铜绿假单胞菌中III型分泌基因的表达,因此将其命名为PtrA(铜绿假单胞菌III型阻遏物A)。已证实PtrA与III型转录激活因子ExsA之间存在直接相互作用,这表明其阻遏功能可能是通过抑制ExsA蛋白功能来实现的。实际上,exsA的表达升高可补偿PtrA的阻遏作用。有趣的是,ptrA的表达受到铜离子的高度特异性诱导。还鉴定出了一种铜响应双组分调节系统copR-copS,它对于铜绿假单胞菌的抗铜性以及响应铜信号激活ptrA至关重要。在小鼠烧伤创面感染期间ptrA的表达升高表明,铜绿假单胞菌已经进化出紧密的调节系统,以响应特定环境信号(如铜胁迫)关闭耗能的III型分泌装置。

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