ROS Y-27632 ROCK inhibitor production after pathogen attack was often accompanied by cell wall protein cross-linking, a reaction able to strengthen this physical barrier and to limit bacterial progression. These two reactions were observed after D. dadantii infection of the resistant abscisic acid-deficient sitiens tomato mutant at the borders of bacteria-infiltrated areas, where bacterial containment was clearly visible. Such protein cross-linking was clearly absent in bos1 infected leaves and this lack might be one of the factors responsible for the more rapid bacterial spreading observed in the mutant. On the other hand, Torres et al. showed that ROS production could suppress cell death in cells surrounding sites of NADPH oxidases activation. This cell death involved the salicylic acid signalisation pathway. Interestingly, as reported during infection with Botrytis, a strong accumulation of the PR1 salicylic acidmarker transcripts was observed in bos1 leaves during D. dadantii infection. We may therefore envision that the lack of early extracellular ROS production in bos1 plants might be involved in the deregulation of necrosis spreading observed later during infection. Interestingly, the bos1 necrotic phenotype looks like that observed with the lesion-mimic lsd1 mutant impaired in a mechanism that protects Arabidopsis cells from death when confronted with oxidative stress signals. Plant cell death in response to pathogen attack has been often associated to ROS production. VE-822 abmole Furthermore, increased ROS sensitivity has been proposed as a common factor in the various aspects of the bos1 phenotype. In B. cinerea-infected Arabidopsis plants, although ROS production could be detected early in the infection, significant ROS increase in bos1 plants became apparent only as disease symptoms began to appear,2 days after inoculation. Similarly, in our pathosystem, intracellular ROS production visualized by DCFH-DA staining was detected in both bos1 and wild type infected leaves 24 hpi with a similar intensity. However, when necrosis appeared, a strong accumulation of ROS that co-localized with necrosis was only observed in the bos1 infected plants. Albeit responses of bos1 plants to both B. cinerea and D. dadantii resulted in increased plant cell death and intracellular ROS production, the outcome of both infections varied drastically. bos1 plants were highly susceptible to the fungus while D. dadantii -induced necrosis provoked an arrest of the maceration and of the bacterial multiplication thus appearing to be an efficient defence mechanism that is exacerbated in the bos1 mutant. It should be noted that, on the contrary, no such effect on bacterial survival was observed after infection of bos1 plants by both virulent and avirulent Pseudomonas syringae strains.