However, as it was previously observed during B. cinerea infection, we observed a much stronger oxidative stress in the bos1 mutant than in the WT after D. Reversine dadantii infection 3 dpi when necrosis started. Intracellular H2O2 accumulation using DCFH-DA staining was still observed in the atrbohD-atrbohF double mutant line indicating that this late ROS production is NADPH oxidase-independent in our pathosystem. Successful infections of compatible pathogens result from a subtle balance between the production of virulence factors and the host responses to pathogen invasion referred to as basal resistance. In addition, pathogens like D. dadantii may colonize their host asymptomatically and intensive multiplication and maceration symptoms only occur when environmental conditions are favourable for disease expression. The fate of symptom production might even be more complex as exemplified by the symptom appearance and progression differences in Saintpaulia – the plant from which the D. dadantii strain used in this study was isolated – and Arabidopsis. In Saintpaulia, there is a checkpoint in the symptom occurrence but, in most plants, once maceration is initiated, rotting proceeds to systemic maceration. In contrast, in Arabidopsis, maceration might stop at different stages during infection and up to 50�C60% of the macerations stop prematurely within the inoculated leaf. This arrest in maceration is usually accompanied by the necrosis of the plant cell layers directly adjacent to the macerated zone. Analysis of the Arabidopsis bos1 mutant revealed a tight control of this plant defence response to D. dadantii infection. The bos1 phenotype associated to the D. dadantii infection is complex, highlighting two contrasting phases of the infection process in Arabidopsis. Indeed, maceration symptoms appeared and developed more rapidly in bos1 as compared to wild type plants and, during the first two days post infection, bos1 plants allowed up to a 10-fold higher bacterial multiplication. However, at later time points, a cell death process – as seen by a trypan blue staining – occurred around the macerated zone in most bos1 plants leading to a necrosis. This necrosis then spread to the whole infected leaf and further systemically to the whole plant. This necrosis was accompanied by a maceration stop and a decrease in bacterial population in the infected area, indicating that this response is effective in stopping infection progression. As observed during B. cinerea infection, BOS1 transcripts accumulated in D. dadantii -infected plants from 12 hours post inoculation. This bos1 activation was specifically dependent on the production and secretion of the PelB and/or PelC pectate lyases. D. dadantii ABT-199 abmole secretes at least eleven pectinases via the type II Out secretion machinery, the five major ones being encoded by the pelA to pelE genes.