The thioredoxin system is of great importance for maintenance of cellular redox homeostasis. Here, we show that it has a severe influence on virulence of Botrytis cinerea, demonstrating that redox processes are important for host-pathogen interactions in this necrotrophic plant pathogen. The thioredoxin system is composed of two enzymes, the thioredoxin and the thioredoxin reductase. We identified two genes encoding for thioredoxins (bctrx1, bctrx2) and one gene encoding for a thioredoxin reductase (bctrr1) in the genome of B. cinerea. Knockout mutants of bctrx1 and bctrr1 were severely impaired in virulence and more sensitive to oxidative stress. Additionally, Δbctrr1 showed enhanced H2O2 production and retarded growth. To investigate the impact of the second major cellular redox system, glutathione, we generated deletion mutants for two glutathione reductase genes. The effects were only marginal; deletion of bcglr1 resulted in reduced germination and, correspondingly, to retarded infection as well as reduced growth on minimal medium, whereas bcglr2 deletion had no distinctive phenotype. In summary, we showed that the balanced redox status maintained by the thioredoxin system is essential for development and pathogenesis of B. cinerea, whereas the second major cellular redox system, the glutathione system, seems to have only minor impact on these processes.
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. Keywords ROS • NADPH oxidases • Thioredoxin • Glutathione • Oxidative stress Reactive Oxygen Species (ROS)Reactive oxygen species (ROS) are generated in all aerobic environments and play a major role for all organisms dependent on oxygen. The oxygen in our atmosphere facilitated the evolution of multi-cellular organisms, but is also the source for several
Important for the lifestyle and survival of every organism is the ability to respond to changing environmental conditions. The necrotrophic plant pathogen Botrytis cinerea triggers an oxidative burst in the course of plant infection and therefore needs efficient signal transduction to cope with this stress. The factors involved in this process and their precise roles are still not well known. Here, we show that the transcription factor Bap1 and the response regulator (RR) B. cinerea Skn7 (BcSkn7) are two key players in the oxidative stress response (OSR) of B. cinerea; both have a major influence on the regulation of classical OSR genes. A yeast-one-hybrid (Y1H) approach proved direct binding to the promoters of gsh1 and grx1 by Bap1 and of glr1 by BcSkn7. While the function of Bap1 is restricted to the regulation of oxidative stress, analyses of ⌬bcskn7 mutants revealed functions beyond the OSR. Involvement of BcSkn7 in development and virulence could be demonstrated, indicated by reduced vegetative growth, impaired formation of reproductive structures, and reduced infection cushion-mediated penetration of the host by the mutants. Furthermore, ⌬bcskn7 mutants were highly sensitive to oxidative, osmotic, and cell wall stress. Analyses of ⌬bap1 bcskn7 double mutants indicated that loss of BcSkn7 uncovers an underlying phenotype of Bap1. In contrast to Saccharomyces cerevisiae, the ortholog of the glutathione peroxidase Gpx3p is not required for nuclear translocation of Bap1. The presented results contribute to the understanding of the OSR in B. cinerea and prove that it differs substantially from that of yeast, demonstrating the complexity and versatility of components involved in signaling pathways.
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