Disturbance of the Ca 2+ /calmodulin‐dependent signalling pathway is responsible for the resistance of Arabidopsis dnd1 against Pectobacterium carotovorum infection

SUMMARY Arabidopsis thaliana wild‐type Col‐0 and its mutant, ‘ defence, no death ’ ( dnd ) 1‐1 , were infected with biotrophic Pseudomonas syringae pv. tomato strain DC3000 and necrotrophic Pectobacterium carotovorum strain KACC 10228, and cellular and molecular responses among them were then analysed. Col‐0 wild‐type was susceptible to both pathogens. By contrast, neither DC3000 nor KACC 10228 infected dnd1‐1 (Yu et al., 1998. Proc. Natl. Acad. Sci. USA 95: 7819–7824). Neither of the pathogens triggered cell death or accumulation of active oxygen species in dnd1‐1 . KACC 10228 induced accelerated transcriptions of PDF1.2 and AtEBP genes in wild‐type Col‐0, while DC3000‐induced transcriptions of them were relatively retarded. Neither of the pathogens modified the constitutive transcription of PR1 in dnd1‐1 . PDF1.2 and AtEBP transcriptions were not induced by the same treatments. Hydrogen peroxide scavengers, catalase and ascorbic acid, and LaCl 3 , an inhibitor of Ca 2+ influx, diminished cell death and protected the wild‐type plant from KACC 10228 infection, while EGTA inhibited cell death and pathogen growth. Exogenous Ca 2+ nullified resistance against KACC 10228 challenge in dnd1‐1 . W‐7 and chloropromazine, two calmodulin antagonists, also triggered cell death in dnd1‐1 and abolished resistance against KACC 10228. In summary, cell death is correlated with KACC 10228 infection and disease development. Furthermore, the resistance of dnd1‐1 against P. carotovorum is dependent on calmodulin and inhibition of cytosolic Ca 2+ increment.