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系统靶向突变食酸菌属 3937 中的 MarR/SlyA 家族成员揭示了 MfbR 在响应酸性 pH 调节毒力基因表达中的作用。

Systematic targeted mutagenesis of the MarR/SlyA family members of Dickeya dadantii 3937 reveals a role for MfbR in the modulation of virulence gene expression in response to acidic pH.

机构信息

Univ Lyon, F-69622 Lyon France.

出版信息

Mol Microbiol. 2010 Nov;78(4):1018-37. doi: 10.1111/j.1365-2958.2010.07388.x. Epub 2010 Sep 27.

DOI:10.1111/j.1365-2958.2010.07388.x
PMID:21062374
Abstract

Pathogenicity of Dickeya dadantii is a process involving several factors, such as plant cell wall-degrading enzymes and adaptation systems to adverse conditions encountered in the apoplast. Regulators of the MarR family control a variety of biological processes, including adaptation to hostile environments and virulence. Analysis of the members of this family in D. dadantii led to the identification of a new regulator, MfbR, which controls virulence. MfbR represses its own expression but activates genes encoding plant cell wall-degrading enzymes. Purified MfbR increases the binding of RNA polymerase at the virulence gene promoters and inhibits transcription initiation at the mfbR promoter. MfbR activity appeared to be modulated by acidic pH, a stress encountered by pathogens during the early stages of infection. Expression of mfbR and its targets, during infection, showed that MfbR is unable to activate virulence genes in acidic conditions at an early step of infection. In contrast, alkalinization of the apoplast, during an advanced stage of infection, led to the potentialization of MfbR activity resulting in plant cell wall degrading enzyme production. This report presents a new example of how pathogens adjust virulence-associated factors during the time-course of an infection.

摘要

迪氏棒形杆菌的致病性是一个涉及多个因素的过程,例如植物细胞壁降解酶和适应质外体中遇到的不利条件的适应系统。MarR 家族的调节剂控制着多种生物过程,包括对恶劣环境的适应和毒力。对 D. dadantii 中该家族成员的分析导致了一种新的调节剂 MfbR 的鉴定,它控制着毒力。MfbR 抑制自身表达,但激活编码植物细胞壁降解酶的基因。纯化的 MfbR 增加了 RNA 聚合酶在毒力基因启动子上的结合,并抑制 mfbR 启动子上的转录起始。MfbR 活性似乎受到酸性 pH 的调节,这是病原体在感染早期阶段遇到的一种应激。在感染过程中 mfbR 和其靶基因的表达表明,在感染的早期阶段,MfbR 无法在酸性条件下激活毒力基因。相比之下,在感染的后期,质外体的碱化导致 MfbR 活性的增强,从而导致植物细胞壁降解酶的产生。本报告提供了一个新的例子,说明病原体如何在感染过程中调整与毒力相关的因素。

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