Three unique mutants of Arabidopsis identify eds loci required for limiting growth of a biotrophic fungal pathogen
Three unique mutants of Arabidopsis identify eds loci required for limiting growth of a biotrophic fungal pathogen
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DOI：
10.1046/j.1365-313x.2000.00870.x
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发表时间：
2000-10-01
期刊：
影响因子：
7.2
通讯作者：
Ausubel, FM
中科院分区：
文献类型：
--
作者：
Dewdney, J;Reuber, TL;Ausubel, FM
为了确定限制生物营养真菌病原体生长的防御反应的组成部分，我们分离了对奥氏白粉菌疾病易感性增强的拟南芥突变体。我们最初的表征集中在三个突变体：eds14、eds15 和 eds16。这些都没有明显更容易受到细菌病原体丁香假单胞菌 pv 的毒力菌株的影响。斑斑 (Psm)。当表达无毒基因 avrRpt2 的 Psm 渗透时，所有三种突变体都会产生过敏反应，该基因通过 RPS2 编码的 LZ-NBS/LRR 抗性蛋白激活抗性。 Psm(avrRpt2) 的生长虽然在突变体中比在野生型中稍大，但小于等基因毒力菌株的生长。这些结果表明通过 LZ-NBS/LRR R 基因介导的抗性是有功能的。对无毒霜霉寄生菌株生长的分析表明，TIR-NBS/LRR R 基因利用的抗性途径在所有三个突变体中也有效。令人惊讶的是，只有 eds14 和 eds16 对菊苣白粉菌更敏感。对 eds14、eds15 和 eds16 中 PR-1、BGL2、PR-5 和 PDF1.2 表达谱的分析揭示了所有品系与野生型的差异。相反，这些突变体与野生型在 E. orontii 渗透位点的胼胝质沉积方面没有显着差异。所有三种突变体在感染后水杨酸水平均降低。 eds16 被定位到 I 号染色体的下臂，通过互补测试发现它与水杨酸缺陷突变体 sid2 等位。
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.