Role of salicylic acid signaling in the biotrophy-necrotrophy transition of <i>Xanthomonas campestris</i> pv. <i>campestris</i> infection in <i>Brassica napus</i>

Abstract

To characterize the hormonal regulations in the transition between biotrophic and necrotrophic phases of Xanthomonas campestris pv. campestris (Xcc) infection, the endogenous phytohormone and reactive oxygen species (ROS) levels and glutathione (GSH) redox status of non-inoculated and Xcc-infected Brassica napus cv. Mosa leaves were measured at various points after inoculation. This time-course study revealed two distinct phases of the Xcc-infection, namely an early asymptomatic (biotrophic) phase that could be observed at 2 days post-inoculation (DPI) and a destructive necrotrophic phase that occurred at 7-24 DPI and was associated with V-shaped necrosis. The length of the V-shaped lesions increased significantly with the progression of infection, as did H2O2 accumulation and the expression of NADPH oxidase. Xcc-infections induced the gradual depression of the reduced/oxidized GSH/GSSG ratio with the progression of disease. Furthermore, Xcc inoculation reduced levels of salicylic acid (SA), jasmonic acid (JA), abscisic acid (ABA), and cytokinin (CK) during the biotrophic phase (at 2 DPI); increased SA level (9.5 fold) and the expression of both SA synthesis-related genes (EDS1 and ICS1) and signaling-related genes (NPR1 and PR1) from the 2 to7 DPI. ABA and CK levels gradually increased during the necrotrophic phase. Interestingly, JA level was either reduced or not significantly affected during the necrotrophic phase of infection. Altogether, these results indicate that, in B. napus, changes in SA-mediated ROS production regulate the transition from the symptomless biotrophic phase of Xcc infection to the destructive necrotrophic phase.