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Autophagy is a ubiquitous vesicular process for protein and organelle recycling in eukaryotes. In plant, autophagy is reported to play pivotal roles in nutrient recycling, adaptation to biotic and abiotic stresses. The role of autophagy in plant immunity remains poorly understood. Several reports showed enhanced susceptibility of different Arabidopsis autophagy mutants ( atg ) to necrotrophic fungal pathogens. Interaction of necrotrophic bacterial pathogens with autophagy is overlooked. We then investigated such interaction by inoculating the necrotrophic enterobacterium  Dickeya dadantii  in leaves of the  atg2  and  atg5  mutants and an  ATG8a  overexpressing line. Overexpressing  ATG8a  enhances plant tolerance to  D. dadantii . While  atg5  mutant displayed similar susceptibility to the WT, the  atg2  mutant exhibited accelerated leaf senescence and enhanced susceptibility upon infection. Both phenotypes were reversed when the  sid2  mutation, abolishing SA signaling, was introduced in the  atg2  mutant. High levels of SA signaling in  atg2  mutant resulted in repression of the jasmonic acid (JA) defense pathway known to limit  D. dadantii  progression in  A. thaliana . We provide evidence that in  atg2  mutant, the disturbed hormonal balance leading to higher SA signaling is the main factor causing increased susceptibility to the  D. dadantii  necrotroph by repressing the JA pathway and accelerating developmental senescence.

Salicylic acid is a key player of Arabidopsis autophagy mutant susceptibility to the necrotrophic bacterium Dickeya dadantii