Аннотация
The necrotrophic fungus Botrytis cinerea rapidly kills host tissue with its secreted proteins and metabolites. Necrotrophs can trigger the hypersensitive response, which is accompanied by reactive oxygen species (ROS) production, but it remains unclear whether this ROS burst promotes or restricts B. cinerea infection. We have combined Arabidopsis RESPIRATORY BURST OXIDASE HOMOLOG D (RBOHD) mutant analysis, luminol-based in vivo assays, and the use of CRISPR/Cas9-generated B. cinerea ROS detoxification mutants to analyze the toxic effect of the ROS burst. In addition, RNA-sequencing, transcript analyses and redox imaging were used to study RBOHD-dependent signaling and redox homeostasis. RBOHD mutants showed slightly increased susceptibility to B. cinerea infection, and the apoplastic ROS burst was found to be dependent on RBOHD. Fungal mutants confirmed the importance of SOD1 and AP1 for ROS detoxification and virulence. Unexpectedly, the transcriptomes of B. cinerea -infected Arabidopsis Col-0 and an activation-impaired RBOHD mutant were highly similar 48 hours after inoculation, providing no evidence for a connection of extracellular ROS production and intracellular ROS-induced transcriptional signaling. Nevertheless, RBOHD activity was found to be involved in the maintenance of cellular redox homeostasis under phytotoxic stress. Our results indicate a protective role of the RBOHD-dependent oxidative burst against B. cinerea , but this can be overcome by the fungus via different ROS detoxification mechanisms.