Does <i>Botrytis cinerea</i> Ignore H₂O₂-Induced Oxidative Stress During Infection? Characterization of <i>Botrytis</i> Activator Protein 1

Botrytis cinerea is a phytopathogen infecting a broad range of plants including strawberries and grapevine. During infection, the necrotrophic fungus is exposed to reactive oxygen species (ROS) released by the oxidative burst, an early plant defense reaction. B. cinerea even produces ROS itself in planta. This raises questions about how the pathogen senses and responds to the host defense reaction and which role the pathogen's oxidative stress response systems play. Functional analysis of the AP-1 transcription factor Bap1 confirmed its role as a pivotal regulator of ROS detoxification in vitro. Macroarray analysis revealed 99 H(2)O(2)-induced Bap1 target genes, of which several genes encoded ROS-degrading enzymes as well as other central components of the cellular redox status. However, Bap1 is not essential for pathogenesis. In planta analyses revealed that the Bap1 target genes were not expressed 2 days postinoculation although H(2)O(2) was detectable, proving that the normal virulence of the Deltabap1 mutant is not due to alternative regulation of the major oxidative stress response system in planta. The fungus obviously does not suffer H(2)O(2)-induced oxidative stress in planta, questioning classical ideas about the role of the oxidative burst in the infection process.