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

被引:190
作者
Dewdney, J
Reuber, TL
Wildermuth, MC
Devoto, A
Cui, JP
Stutius, LM
Drummond, EP
Ausubel, FM
机构
[1] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA
[2] Harvard Univ, Sch Med, Dept Genet, Boston, MA USA
[3] Sainsbury Lab, Norwich NR4 7UH, Norfolk, England
[4] Harvard Univ, Dept Organism & Evolutionary Biol, Cambridge, MA 02138 USA
[5] Harvard Univ, Cambridge, MA USA
关键词
defense response; plant-pathogen interactions; disease susceptibility; Arabidopsis; Erysiphe orontii; mutant;
D O I
10.1046/j.1365-313x.2000.00870.x
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
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.
引用
收藏
页码:205 / 218
页数:14
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