Abstract

Research has demonstrated that the interaction between HrpN and the mitochondrial electron transport chain (ETC) causes the generation of the reactive oxygen species (ROS) and an oxidative burst in host cells. To date, the interaction between bacterial infection and host chloroplasts has not been studied. This research was carried out to study the role of chloroplast ETC in this interaction in two host species, apple (Malus x domestica Borkh.) and pear (Pyrus communis L.). Accordingly, apple rootstocks, 'MM-111' (tolerant) and 'MM-106' (susceptible) and pear cultivars, 'Harrow Sweet' (tolerant) and 'Spadona' (susceptible) were micropropagated. Uracil was used as chloroplast ETC inhibitor at the presence and absence of sucrose to compare effects of ETC inhibition both in low and high photosynthesis activity of in vitro shootlets. E. amylovora Ea273 was used for basal inoculation of shootlets and the disease progression was studied by establishing necrosis indices. The in vitro system was initially optimized on 'MM-111' apple. Shoots were exposed to uracil prior to inoculation, in the absence of sucrose to separated herbicide effects of uracil from bacterial necrosis in ETC activated chloroplasts. Uracil on activated ETC chloroplasts and in the presence of E. amylovora, delayed necrosis appearance, the visible symptoms of oxidative burst in shootlets of both hosts. Uracil presence significantly reduced ROS generation during pathogen-host interaction, and ROS generation corresponded with the appearance of necrosis in all cultivars.

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