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.