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Dickeya dadantii  is a broad host range phytopathogenic bacterium provoking soft rot disease on many plants including  Arabidopsis . We showed that, after  D. dadantii  infection, the expression of the  Arabidopsis BOS1  gene was specifically induced by the production of the bacterial PelB/C pectinases able to degrade pectin. This prompted us to analyze the interaction between the  bos1  mutant and  D. dadantii . The phenotype of the infected  bos1  mutant is complex. Indeed, maceration symptoms occurred more rapidly in the  bos1  mutant than in the wild type parent but at a later stage of infection, a necrosis developed around the inoculation site that provoked a halt in the progression of the maceration. This necrosis became systemic and spread throughout the whole plant, a phenotype reminiscent of that observed in some lesion mimic mutants. In accordance with the progression of maceration symptoms, bacterial population began to grow more rapidly in the  bos1  mutant than in the wild type plant but, when necrosis appeared in the  bos1  mutant, a reduction in bacterial population was observed. From the plant side, this complex interaction between  D. dadantii  and its host includes an early plant defence response that comprises reactive oxygen species (ROS) production accompanied by the reinforcement of the plant cell wall by protein cross-linking. At later timepoints, another plant defence is raised by the death of the plant cells surrounding the inoculation site. This plant cell death appears to constitute an efficient defence mechanism induced by  D. dadantii  during  Arabidopsis  infection.

Analysis of the Plant bos1 Mutant Highlights Necrosis as an Efficient Defence Mechanism during D. dadantii/Arabidospis thaliana Interaction