Hommais Florence, Oger-Desfeux Christine, Van Gijsegem Frédérique, Castang Sandra, Ligori Sandrine, Expert Dominique, Nasser William, Reverchon Sylvie
CNRS UMR 5240 Microbiologie, Adaptation et Pathogénie, Université Lyon 1, Bâtiment André Lwoff, 10 rue Raphaël Dubois, F-69622 Villeurbanne Cedex, France.
J Bacteriol. 2008 Nov;190(22):7508-22. doi: 10.1128/JB.00553-08. Epub 2008 Sep 12.
Pathogenicity of the enterobacterium Erwinia chrysanthemi (Dickeya dadantii), the causative agent of soft-rot disease in many plants, is a complex process involving several factors whose production is subject to temporal regulation during infection. PecS is a transcriptional regulator that controls production of various virulence factors. Here, we used microarray analysis to define the PecS regulon and demonstrated that PecS notably regulates a wide range of genes that could be linked to pathogenicity and to a group of genes concerned with evading host defenses. Among the targets are the genes encoding plant cell wall-degrading enzymes and secretion systems and the genes involved in flagellar biosynthesis, biosurfactant production, and the oxidative stress response, as well as genes encoding toxin-like factors such as NipE and hemolysin-coregulated proteins. In vitro experiments demonstrated that PecS interacts with the regulatory regions of five new targets: an oxidative stress response gene (ahpC), a biosurfactant synthesis gene (rhlA), and genes encoding exported proteins related to other plant-associated bacterial proteins (nipE, virK, and avrL). The pecS mutant provokes symptoms more rapidly and with more efficiency than the wild-type strain, indicating that PecS plays a critical role in the switch from the asymptomatic phase to the symptomatic phase. Based on this, we propose that the temporal regulation of the different groups of genes required for the asymptomatic phase and the symptomatic phase is, in part, the result of a gradual modulation of PecS activity triggered during infection in response to changes in environmental conditions emerging from the interaction between both partners.
菊欧文氏菌（现称达旦氏果胶杆菌）是许多植物软腐病的病原体，其致病性是一个复杂的过程，涉及多个因素，这些因素的产生在感染过程中受到时间调控。PecS是一种转录调节因子，可控制多种毒力因子的产生。在此，我们利用微阵列分析来确定PecS调控子，并证明PecS显著调控了一系列与致病性相关的基因以及一组与逃避宿主防御有关的基因。其靶标包括编码植物细胞壁降解酶和分泌系统的基因、参与鞭毛生物合成、生物表面活性剂产生和氧化应激反应的基因，以及编码毒素样因子（如NipE和溶血素共调节蛋白）的基因。体外实验表明，PecS与五个新靶标的调控区域相互作用：一个氧化应激反应基因（ahpC）、一个生物表面活性剂合成基因（rhlA），以及编码与其他植物相关细菌蛋白相关的输出蛋白的基因（nipE、virK和avrL）。pecS突变体比野生型菌株更迅速、更有效地引发症状，这表明PecS在从无症状阶段到有症状阶段的转变中起关键作用。基于此，我们提出，无症状阶段和有症状阶段所需的不同基因组的时间调控，部分是由于感染期间响应双方相互作用中出现的环境条件变化而触发的PecS活性逐渐调节的结果。
