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Three unique mutants of Arabidopsis identify eds loci required for limiting growth of a biotrophic fungal pathogen
Article first published online: 25 DEC 2001
The Plant Journal
Volume 24, Issue 2, pages 205–218, October 2000
How to Cite
Dewdney, J., Reuber, T. L., Wildermuth, M. C., Devoto, A., Cui, J., Stutius, L. M., Drummond, E. P. and Ausubel, F. M. (2000), Three unique mutants of Arabidopsis identify eds loci required for limiting growth of a biotrophic fungal pathogen. The Plant Journal, 24: 205–218. doi: 10.1046/j.1365-313x.2000.00870.x
- Issue published online: 25 DEC 2001
- Article first published online: 25 DEC 2001
- Received 10 April 2000; revised 4 August 2000; accepted 7 August 2000.
- defense response;
- plant–pathogen interactions;
- disease susceptibility;
- Erysiphe orontii;
To identify components of the defense response that limit growth of a biotrophic fungal pathogen, we isolated Arabidopsis mutants with enhanced disease susceptibility to Erysiphe orontii. Our initial characterization focused on three mutants, eds14, eds15, and eds16. None of these is considerably more susceptible to a virulent strain of the bacterial pathogen Pseudomonas syringae pv. maculicola (Psm). All three mutants develop a hypersensitive response when infiltrated with Psm expressing the avirulence gene avrRpt2, which activates resistance via the LZ-NBS/LRR resistance protein encoded by RPS2. 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. These results indicate that resistance mediated via LZ-NBS/LRR R genes is functional. 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 more susceptible to Erysiphe cichoracearum. Analysis of the expression profiles of PR-1, BGL2, PR-5 and PDF1.2 in eds14, eds15, and eds16 revealed differences 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 chromosome I and found by complementation tests to be allelic to the salicylic acid-deficient mutant sid2.