title: PecS is a global regulator of the symptomatic phase in the phytopathogenic bacterium Erwinia chrysanthemi 3937.
abstract: 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.
authors.affiliation: CNRS UMR 5240 Microbiologie, Adaptation et Pathogénie, Université Lyon 1, Bâtiment André Lwoff, 10 rue Raphaël Dubois, F-69622 Villeurbanne Cedex, France.
authors.forename: Florence
authors.initials: F
authors.lastname: Hommais
authors.forename: Christine
authors.initials: C
authors.lastname: Oger-Desfeux
authors.forename: Frédérique
authors.initials: F
authors.lastname: Van Gijsegem
authors.forename: Sandra
authors.initials: S
authors.lastname: Castang
authors.forename: Sandrine
authors.initials: S
authors.lastname: Ligori
authors.forename: Dominique
authors.initials: D
authors.lastname: Expert
authors.forename: William
authors.initials: W
authors.lastname: Nasser
authors.forename: Sylvie
authors.initials: S
authors.lastname: Reverchon
mesh_terms: D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D018983:DNA Footprinting; D016974:Dickeya chrysanthemi / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D024202:Electrophoretic Mobility Shift Assay; D015964:Gene Expression Regulation, Bacterial; D054884:Host-Pathogen Interactions; D019684:Magnoliopsida / Q000382:microbiology*; D009154:Mutation; D020411:Oligonucleotide Array Sequence Analysis; D018384:Oxidative Stress; D011401:Promoter Regions, Genetic / Q000235:genetics; D011485:Protein Binding; D012097:Repressor Proteins / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017422:Sequence Analysis, DNA
chemical_list: D001426:Bacterial Proteins; D012097:Repressor Proteins; C088080:pecS protein, Erwinia chrysanthemi
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