J Bacteriol 2003,185(3):1071–1081.CrossRefPubMed

56. Whiteley M, Bangera MG, Bumgarner RE, Parsek MR, Teitzel GM, Lory S, Greenberg EP: Gene expression in Pseudomonas aeruginosa biofilms. Nature 2001,413(6858):860–864.CrossRefPubMed 57. Danese PN, Silhavy TJ: CpxP, a stress-combative member of the Cpx regulon. J Bacteriol 1998,180(4):831–839.PubMed 58. Potvin E, Sanschagrin F, Levesque RC: Sigma factors in Pseudomonas aeruginosa. FEMS Microbiol Rev 2008,32(1):38–55.CrossRefPubMed 59. Cuny C, Lesbats M, Dukan S: Induction of a global stress response during the first step of Escherichia coli plate growth. Appl learn more Environ Microbiol 2007,73(3):885–889.CrossRefPubMed 60. Mohamed JA, Huang W, Nallapareddy SR, Teng F, Murray BE: Influence of origin of isolates, especially endocarditis isolates, and various genes Fosbretabulin on biofilm formation by Enterococcus faecalis. Infect Immun 2004,72(6):3658–3663.CrossRefPubMed 61. Campbell JH, Pappenheimer AM Jr: Quantitative

studies of the specifiCity of anti-pneumococcal polysaccharide antibodies, types 3 and 8. II. Inhibition of precipitin reactions with oligosaccharides isolated from hydrolysates of S3 and S8. Immunochemistry 1966,3(3):213–222.CrossRefPubMed 62. Adam O, Vercellone A, Paul F, Monsan PF, Puzo G: A nondegradative route for the removal of endotoxin Neuronal Signaling inhibitor from exopolysaccharides. Anal Biochem 1995,225(2):321–327.CrossRefPubMed 63. Bolstad BM, Irizarry RA, Astrand M, Speed TP: A comparison of normalization methods for high density oligonucleotide array data based on variance and bias. Bioinformatics 2003,19(2):185–193.CrossRefPubMed Authors’ contributions TY, TF and CM carried out the phenotype characterization and microarray analysis, and drafted the manuscript. KY and CS performed RT-PCR. NM and HN screened a culture collection of strain 17 for the ability to produce viscous material. TN participated in the analysis of microarray data. CBW, KPL, and HF participated

in the design of this study and drafted the manuscript.”
“Background Citrus canker is a disease caused by the phytopathogens Xanthomonas citri subsp. citri, X. fuscans subsp. aurantifolli and X. alfalfae subsp. citrumelonis [1]. Among the three phytopathogens, the Asiatic form (X. citri subsp. citri), which causes citrus bacterial canker type A, is the most widely spread CYTH4 and severe, attacking all citrus varieties [2]. In Brazil, form A is the most important, being found in practically all areas where citrus canker has been detected [3]. Similarly to most phytobacterioses, there is no efficient way to control citrus canker. The only way to eliminate the disease is through the eradication of sick plants, a procedure that brings significant economical losses. By law, in São Paulo State, the main citrus production area in Brazil, it is mandated to eliminate all plants around the focus of infection in a 30 m radius if the contaminated plants are less than 0.