Fig. 1

prc of X. campestris pv. campestris controls virulence and stress resistance. a Schematic view of the secondary structure of the Prc protein. Domain names are according to the pfam database. b Prc is located in bacterial periplasm and cytosol. Western blotting was used to detect Prc proteins in different cellular fractions. TCP total cellular protein. Western blotting of the membrane-bound and cytosolic proteins VgrS and HPPK, respectively, were used as controls. The experiment was repeated three times. c The inactivation of prc caused a deficiency in virulence. Bacterial strains were inoculated into leaves of the host plant B. oleraceae cv. Jingfeng No. 1. Virulence scores were estimated 10 d after inoculation. Sterile 10 mM MgCl₂ was used as the negative control. d Virulence scores of bacterial strains as shown in c. The virulence levels of bacterial strains were estimated using a semi-quantitative standard. Asterisks indicate significant differences relative to the WT strain (Student's t-test, P < 0.05, n = 12). The result of the in planta growth assay is shown in Supplementary Fig. 2. e and f The prc mutant is sensitive to various antibiotics, including erythromycin e and kanamycin f. In both e and f, the inhibitory zones of antibiotics are shown. The minimal inhibition concentrations (MICs) of the antibiotics were measured and are listed below. Each experiment was repeated three times. g The inactivation of prc resulted in hypersensitivity to iron stress. Bacterial strains were grown on NYG agar containing 2.5 mM FeSO₄ plus 0.5 mM vitamin C for 72 h at 28 °C. The experiment was repeated three times. h The inactivation of prc resulted in hypersensitivity to osmostress. Bacterial strains were grown on NYG agar containing 1.0 M sorbitol for 72 h at 28 °C. The experiment was repeated three times