Reactive oxygen species in the Botrytis - Host interaction

Abstract

Reactive oxygen species (ROS) are unavoidable byproducts of several metabolic processes. Due to their high reactivity they can cause molecular damages such as protein oxidations or DNA mutations, but they also serve as important signalling molecules within cells. Intracellular ROS primarily originate in the mitochondria; however enzymatic ROS generating systems such as the membrane associated NADPH oxidase complex (Nox) contribute to their production. In particular, during host-pathogen interactions ROS are of key importance for plant defence but also for fungal attack. As an early response to pathogen infestation the plant releases high amounts of reactive oxygen species to counteract the pathogen, known as the oxidative burst. It was shown that Botrytis exploits this plant defence reaction and even contributes to this oxidative burst by forming its’ own ROS. Thus, the fungus needs a robust oxidative stress responsive (OSR) system to cope with ROS. In order to balance the intracellular redox state, effective antioxidant systems, including the thioredoxin and the glutathione system, are indispensable. Furthermore, catalases, superoxide dismutases and several peroxidases support ROS scavenging by enzymatic inactivation. Transcription factors such as the Botrytis activator protein (Bap1) and the response regulator Skn7 were shown to be involved in OSR. In this chapter we discuss the role of ROS in Botrytis - host interaction and both ROS generating and detoxifying systems and their importance for Botrytis pathogenicity.