Absence of Cu-Zn superoxide dismutase BCSOD1 reduces Botrytis cinerea virulence in Arabidopsis and tomato plants, revealing interplay among reactive oxygen species, callose and signalling pathways.

ABSTRACT: Plants activate responses against pathogens, including the oxidative burst. Necrotrophic pathogens can produce reactive oxygen species (ROS) that benefit the colonization process. Previously, we have demonstrated that tomato plants challenged with Botrytis cinerea accumulate ROS and callose, together with the induction of genes involved in defence, signalling and oxidative metabolism. Here, we studied the infection phenotype of the ?bcsod1 strain in both tomato and Arabidopsis plants. This mutant lacks bcsod1, which encodes Cu-Zn superoxide dismutase (SOD). This enzyme catalyses the conversion of superoxide ion ( O2-) into hydrogen peroxide (H₂ O₂ ). ROS play a protective role and act as signals in plants. ?bcsod1 displayed reduced virulence compared with wild-type B05.10 in both species. Plants infected with ?bcsod1 accumulated less H₂ O₂ and more O2- than those infected with B05.10, which is associated with an increase in the defensive polymer callose. This supports a major role of fungal SOD in H₂ O₂ production during the plant-pathogen interaction. The early induction of the callose synthase gene PMR4 suggested that changes in ROS altered plant defensive responses at the transcriptional level. The metabolites and genes involved in signalling and in response to oxidative stress were differentially expressed on ?bcsod1 infection, supporting the notion that plants perceive changes in ROS balance and activate defence responses. A higher O₂^- /H₂ O₂ ratio seems to be beneficial for plant protection against this necrotroph. Our results highlight the relevance of callose and the oxylipin 12-oxo-phytodienoic acid (OPDA) in the response to changes in the oxidative environment, and clarify the mechanisms that underlie the responses to Botrytis in Arabidopsis and tomato plants.

SUBMITTER: Lopez-Cruz J 

PROVIDER: S-EPMC6638242 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature