PecS Is a Global Regulator of the Symptomatic Phase in the Phytopathogenic Bacterium Erwinia chrysanthemi 3937
PecS Is a Global Regulator of the Symptomatic Phase in the Phytopathogenic Bacterium Erwinia chrysanthemi 3937
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DOI：
10.1128/jb.00553-08
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发表时间：
2008-11-01
影响因子：
3.2
通讯作者：
Reverchon, Sylvie
中科院分区：
文献类型：
--
作者：
Hommais, Florence;Oger-Desfeux, Christine;Reverchon, Sylvie
菊花Erwinia菊花肠杆菌（Dickeya dadantii）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，其产生受感染期间的时间调节。PecS是一种转录调节剂，控制各种毒力因子的产生。在这里，我们使用微阵列分析来定义PecS调控子，并证明PecS显著调控一系列可能与致病性相关的基因和一组与逃避宿主防御有关的基因。靶点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、生物表面活性剂生产和氧化应激反应的基因，以及编码NipE和溶血素协同调节蛋白等毒素样因子的基因。体外实验表明，PecS与五个新靶点的调控区域相互作用：氧化应激反应基因（ahpC）、生物表面活性剂合成基因（rhlA）和编码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在从无症状期到有症状期的转换中起着关键作用。基于此，我们提出无症状期和症状期所需的不同基因组的时间调节部分是在感染期间响应双方相互作用产生的环境条件变化而触发的PecS活性逐渐调节的结果。
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.