Tricking the Guard: Exploiting Plant Defense for Disease Susceptibility

被引:149
作者
Lorang, J. [1 ,2 ]
Kidarsa, T. [1 ,2 ]
Bradford, C. S. [1 ,2 ]
Gilbert, B. [1 ,2 ]
Curtis, M. [1 ,2 ]
Tzeng, S. -C. [3 ]
Maier, C. S. [3 ]
Wolpert, T. J. [1 ,2 ]
机构
[1] Oregon State Univ, Dept Bot & Plant Pathol, Corvallis, OR 97331 USA
[2] Oregon State Univ, Ctr Genome Res & Biocomp, Corvallis, OR 97331 USA
[3] Oregon State Univ, Dept Chem, Corvallis, OR 97331 USA
基金
英国生物技术与生命科学研究理事会;
关键词
HOST-SELECTIVE TOXINS; VICTORIN SENSITIVITY; RESISTANCE GENE; THIOREDOXIN H5; LRR GENE; ARABIDOPSIS; PROTEINS; FEATURES;
D O I
10.1126/science.1226743
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Typically, pathogens deploy virulence effectors to disable defense. Plants defeat effectors with resistance proteins that guard effector targets. We found that a pathogen exploits a resistance protein by activating it to confer susceptibility in Arabidopsis. The guard mechanism of plant defense is recapitulated by interactions among victorin (an effector produced by the necrotrophic fungus Cochliobolus victoriae), TRX-h5 (a defense-associated thioredoxin), and LOV1 (an Arabidopsis susceptibility protein). In LOV1's absence, victorin inhibits TRX-h5, resulting in compromised defense but not disease by C. victoriae. In LOV1's presence, victorin binding to TRX-h5 activates LOV1 and elicits a resistance-like response that confers disease susceptibility. We propose that victorin is, or mimics, a conventional pathogen virulence effector that was defeated by LOV1 and confers virulence to C. victoriae solely because it incites defense.
引用
收藏
页码:659 / 662
页数:4
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