Abstract

Alternaria brassicae is a necrotrophic fungal pathogen capable of infecting most of the agriculturally important Brassica species. The mechanisms underlying invasion of A. brassicae and host responses are unknown. In the present study, we exploited the natural variation in Arabidopsis to understand the molecular and cellular mechanisms underlying resistance to A. brassicae. Using a subset of resistant (Ei-2, Ull2-3, Lz-0, and Cvi-0) and susceptible (Gre-0, Est-1, and Zdr1) accessions, we show that the susceptibility to A. brassicae is associated with higher ROS accumulation and cell death. Susceptibility to A. brassicae was reduced in the rboh (D, E and F) mutants that are incapable of producing ROS, suggesting that RBOH D, E and F may act as negative regulators of defence against this pathogen. Additionally, our data also supports the hypothesis that the Jasmonic acid (JA), Ethylene (ET) and Abscisic acid (ABA) signalling pathways positively contribute to resistance against necrotrophic pathogens. In summary, these results reveal the central role of ROS and cell death in the pathogenesis of A. brassicae and expand our understanding of plant-necrotroph interactions.

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