Three unique mutants of Arabidopsis identify eds loci required for limiting growth of a biotrophic fungal pathogen

To identify components of the defense response that limit growth of a biotr ophic fungal pathogen, we isolated Arabidopsis mutants with enhanced diseas e susceptibility to Erysiphe orontii. Our initial characterization focused on three mutants, eds14, eds15, and eds16. None of these is considerably mo re susceptible to a virulent strain of the bacterial pathogen Pseudomonas s yringae pv. maculicola (Psm). All three mutants develop a hypersensitive re sponse when infiltrated with Psm expressing the avirulence gene avrRpt2, wh ich activates resistance via the LZ-NBS/LRR resistance protein encoded by R PS2. The growth of Psm(avrRpt2), while somewhat greater in the mutants than in the wild type, is less than growth of the isogenic virulent strain. The se results indicate that resistance mediated via LZ-NBS/LRR R genes is func tional. Analysis of the growth of avirulent Peronospora parasitica strains showed that the resistance pathway utilized by TIR-NBS/LRR R genes is also operative in all three mutants. Surprisingly, only eds14 and eds16 were mor e susceptible to Erysiphe cichoracearum. Analysis of the expression profile s of PR-1, BGL2, PR-5 and PDF1.2 in eds14, eds15, and eds16 revealed differ ences from the wild type for all the lines. In contrast, these mutants were not significantly different from wild type in the deposition of callose at sites of E. orontii penetration. All three mutants have reduced levels of salicylic acid after infection. eds16 was mapped to the lower arm of chromo some I and found by complementation tests to be allelic to the salicylic ac id-deficient mutant sid2.