The role of reactive oxygen species (ROS) in development and pathogenicity of phytopathogenic fungi

Basic data for this project

Description

The role of reactive oxygen species in defense against pathogens has been studied in detail in animal and plant systems; in plants the oxidative burst, a fast transient increase in ROS level has major impact on first-line defense (strengthening of cell walls) and induction of defense genes. In this project the impact of ROS generation and scavenging was studied in two model systems, pathogenic fungi with different strategies: the necrotrophic pathogen Botrytis cinerea (causing grey mould in more than 200 host plants) produces a massive oxidative burst and grows on dead tissue, whereas Claviceps purpurea (causing Ergot disease on grasses and cereals) is a biotrophic fungus causing (almost) no host defense reactions. Functional analyses (targeted gene inactivation; expression studies) revealed several unexpected results: • The stress-activated MAPK pathway (hog-type) is essential for virulence in both fungi; however, the funtion of downstream transcription factors (Atf1) and upstream components (histidine kinases) is significantly different. • Though B. cinerea causes a significant oxidative burst in planta, the central oxidative stress response system (Bap1) is not active, i.e. the fungus obviously does not “sense” oxidative stress; this strongly suggests that the oxidative burst has no major direct impact on the pathogen but has mainly signalling function. • In both fungi the NADPH oxidase complexes are of central importance for development and pathogenicity, but their roles differ considerably: in contrast to C. purpurea, in B. cinerea Nox activity is essential for penetration; whereas in C. purpurea the Nox complex seems to be important for a balanced interaction: a mutant lacking one Nox subunit is even more virulent. These data indicate that in both fungi the same, highly conserved “equipment” is used quite differently, conform to the different life style.