To investigate whether this mutant could be affected during D. dadantii infection, we analysed the disease symptoms produced on the bos1 mutant after low bacterial inoculum deposition on wounded leaves. On Col-0 wild type plants, typical soft rot usually developed spreading to the whole infected leaf, but in some cases, a DAPT Gamma-secretase inhibitor chlorosis appeared around the maceration zone forming a yellow ring. In the bos1 mutant such a chlorosis developed in almost all cases, expanded to the whole infected leaf and spread systemically to the whole plant leading to a complete death of bos1 mutants. This chlorosis always turned into necrosis. The systemic necrosis of infected plants was not observed either after Navitoclax non-pathogenic enterobacterium inoculation or after B. cinerea mycelium application. This indicated that a specific factor associated to D. dadantii might trigger this necrotic response. The role that this necrotic response to D. dadantii inoculation might play in disease development has been analyzed by quantifying maceration symptoms, necrosis occurrence and bacterial growth in bos1 and Col-0 plants. After inoculation with a 5 ml drop of a 104 cfu/mL bacterial suspension, soft rot symptoms developed during the first 2 dpi in both genotypes but significantly faster in bos1 leaves than in WT. Necrosis around the maceration zone developed from the second dpi in both genotypes but less frequently in Col-0 than in bos1. In wild type plants however, this necrosis always stayed restricted to the few plant cells surrounding the rotted tissue. In contrast, in bos1 plants, the necrosis expanded to the whole infected leaves from 3 dpi onwards and affected rapidly the whole plant in most cases. This necrosis symptom was concomitant with an arrest of soft rot expansion and a drying of the maceration zone so that from the third dpi onwards, maceration symptoms did not evolve on the bos1 mutant and the soft rot did not expand to more than one half of the infected leaves except in a few cases. In contrast, maceration continued to progress in WT leaves leading to the complete rotting of more than 40% of infected leaves at 6 dpi. To evaluate the consequence of necrosis on the infecting bacterial population, bacterial growth was monitored in planta in both genotypes. One day post inoculation, a 100-fold multiplication was observed in both genotypes. Two dpi, about 10-fold more bacteria were found in bos1 infected leaves compared to wild type ones. On the contrary, a further increase in bacterial population was observed 3 dpi in wild type infected leaves while the number of bacteria declined in bos1 leaves, correlating with the halt of maceration expansion and the appearance of the necrosis. In all chlorotic or necrotic systemic leaves tested, we never detected the presence of bacteria except for the rare leaves exhibiting maceration symptoms.