Alternaria leaf blight, a disease of oilseed Brassicas is caused by a necrotrophic phytopathogenic fungus . The details of its pathogenesis and defence responses elicited in the host upon infection have not been thoroughly investigated. Here, accession Gre-0 was identified to be highly susceptible to . A comparative histopathological analysis for disease progression and plant responses to in and revealed significant similarities between the two compatible pathosystems. Interestingly, in both the compatible hosts, ROS accumulation, cell death and callose deposition correlated with the development of the disease. Based on our results we propose that - can be an apt model pathosystem since it emulates the dynamics of the pathogen interaction with its natural host- Brassicas. The existing genetic diversity in can be a starting point to screen for variation in responses to Alternaria leaf blight. Furthermore, several tools available for can facilitate the dissection of genetic and molecular basis of resistance.

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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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