Study of incompatible Arabidopsis thaliana-Botrytis cinerea interactions to identify plant responses that may lead to increased resistance to the pathogen
Final Report Abstract
The ascomycetous fungus Botrytis cinerea is the causal agent of gray mold diseases in more than 235 plant species. The fungus is a typical necrotroph whose infection cycle includes the induction of plant cell death followed by the maceration of the plant tissue and reproduction by forming asexual spores on the rotted plant material. Disease symptoms depend on the host plant, the infected part of the plant and the environmental conditions. In general, B. cinerea is responsible for severe economic losses that are either due to the damage of growing plants in the field or the rot of harvested fruits, flowers and vegetables during storage under cold and humid conditions. Remarkably, the fungus might be hidden in the plant or the crops due to a latent or quiescent phase (growth without causing symptoms) and is therefore difficult to detect in the field and at the time of selling. Quiescent infections (incompatible interactions) are supposed to be transient and to pass over into parasitic infections (compatible fungus-host interaction) due to so far unknown environmental cues affecting the pathogen, the host or both. The nature of incompatible interactions is likely complex basing on a finely tuned equilibrium between fungal virulence and plant defense. Implicated processes in host resistance to B. cinerea are related to the regulation of cell death, plant hormone biosynthesis and signaling, and production of antifungal compounds. In the project, a set of virulence-attenuated B. cinerea strains (natural isolates and mutants obtained by targeted inactivation) were used for the more detailed characterization of the fungus-host interaction using different genotypes of the model plant Arabidopsis thaliana. Wildtype plants (Col-0) can be readily infected by B. cinerea; however, A. thaliana as other Brassicaceae exhibits a high basal resistance towards this pathogen. Fungus-host combinations resulting in incompatible interactions (no or restricted infection) can be either due to a less virulent pathogen or a more resistant plant. The B. cinerea mutant (Δbcvel1) deleted for the gene encoding a fungal specific regulator of light signaling and secondary metabolism was found to strike up incompatible interactions with different A. thaliana genotypes such as Col-0 and the more susceptible line gw33. The restriction of pathogen growth is associated by an increased accumulation of reactive oxygen species (superoxide, hydrogen peroxide) as established by NBT and DAB staining of infected plant tissues suggesting an untimely and/ or over-stimulation of host defense responses. Expression profiles of pathogenesis-related genes in both interaction partners i.e. plant PR genes and known fungal virulence factors are currently evaluated.
