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Journal of Bacteriology, November 2008, p. 7508-7522, Vol. 190, No. 22
0021-9193/08/$08.00+0     doi:10.1128/JB.00553-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

PecS Is a Global Regulator of the Symptomatic Phase in the Phytopathogenic Bacterium Erwinia chrysanthemi 3937{triangledown} ,{dagger}

Florence Hommais,1 Christine Oger-Desfeux,2 Frédérique Van Gijsegem,3 Sandra Castang,1,{ddagger} Sandrine Ligori,3 Dominique Expert,3 William Nasser,1 and Sylvie Reverchon1*

CNRS UMR 5240 Microbiologie, Adaptation et Pathogénie, INSA de Lyon, Université Lyon 1, Bâtiment André Lwoff, 10 rue Raphaël Dubois, F-69622 Villeurbanne CEDEX, France,1 Pôle Rhône-Alpes de Bioinformatique, IFR41, Université Lyon 1, Bâtiment Gregor Mendel, 16 rue Dubois, F-69622 Villeurbanne CEDEX, France,2 Laboratoire Interactions Plantes Pathogènes, UMR 217 INRA/AgroParisTech/UPMC P6, 16 rue Claude Bernard, 75231 Paris CEDEX 05, France3

Received 22 April 2008/ Accepted 1 August 2008

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.

* Corresponding author. Mailing address: CNRS UMR 5240 Microbiologie, Adaptation et Pathogénie, Université Lyon 1, Bâtiment André Lwoff, 10 rue Raphaël Dubois, F-69622 Villeurbanne CEDEX, France. Phone: 33 4 72 43 26 95. Fax: 33 4 72 43 15 84. E-mail: sylvie.reverchon-pescheux{at}insa-lyon.fr

{triangledown} Published ahead of print on 12 September 2008.

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.

{ddagger} Present address: Children's Hospital Boston, Division of Infectious Diseases, Enders Building, Room 750.5, 300 Longwood Avenue, Boston, MA 02115.

Journal of Bacteriology, November 2008, p. 7508-7522, Vol. 190, No. 22
0021-9193/08/$08.00+0     doi:10.1128/JB.00553-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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