CpxRA双组分系统抑制产肠毒素大肠杆菌热不稳定毒素的基因表达。

IF 2.4 4区 医学 Q3 MICROBIOLOGY
Diana Rodríguez-Valverde, Nancy León-Montes, Tania Siqueiros-Cendón, Sandra Rivera-Gutiérrez, Miguel A Ares, Miguel A De la Cruz
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引用次数: 0

摘要

产肠毒素大肠杆菌(ETEC)菌株至少产生两种肠毒素中的一种:热不稳定(LT)和热稳定(ST)毒素,它们导致水样分泌性腹泻,这是人类ETEC感染的一个标志。一个控制致病菌毒力基因转录的调控系统是CpxRA双组分系统(TCS)。我们报道了编码LT的A和B亚基的eltAB双电子操纵子,通过直接结合CpxR-P在eltAB转录起始位点的-12至+6 bp处抑制CpxRA TCS。此外,cpx应答激活下调了eltAB基因的转录,并且这种负作用依赖于cpxra。我们的数据表明,CpxRA TCS是ETEC主要毒力决定因素之一的LT的负调节因子。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The CpxRA two-component system represses gene expression of the heat-labile toxin of enterotoxigenic Escherichia coli.

Enterotoxigenic Escherichia coli (ETEC) strains produce at least one of two types of enterotoxins: the heat-labile (LT) and heat-stable (ST) toxins, which are responsible for the watery secretory diarrhoea that is a hallmark of the human ETEC infection. One regulatory system that controls the transcription of virulence genes in pathogenic bacteria is the CpxRA two-component system (TCS). We reported that the eltAB bicistronic operon, which encodes for the A and B subunits of LT, was repressed for the CpxRA TCS by direct binding of CpxR-P from -12 to +6 bp with respect to the transcription start site of eltAB. Moreover, the Cpx-response activation down-regulated the transcription of eltAB genes, and this negative effect was CpxRA-dependent. Our data show that CpxRA TCS is a negative regulator of the LT, one of the main virulence determinants of ETEC.

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来源期刊
Journal of medical microbiology
Journal of medical microbiology 医学-微生物学
CiteScore
5.50
自引率
3.30%
发文量
143
审稿时长
4.5 months
期刊介绍: Journal of Medical Microbiology provides comprehensive coverage of medical, dental and veterinary microbiology, and infectious diseases. We welcome everything from laboratory research to clinical trials, including bacteriology, virology, mycology and parasitology. We publish articles under the following subject categories: Antimicrobial resistance; Clinical microbiology; Disease, diagnosis and diagnostics; Medical mycology; Molecular and microbial epidemiology; Microbiome and microbial ecology in health; One Health; Pathogenesis, virulence and host response; Prevention, therapy and therapeutics
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