主页 文献库文献详情
PMID: 18980653 已发表 · ppublish 英语

The Pseudomonas syringae type III effector AvrRpm1 induces significant defenses by activating the Arabidopsis nucleotide-binding leucine-rich repeat protein RPS2.

The Plant journal : for cell and molecular biology ·第 57 卷 ·第 4 期 ·2009-02-27

Kim Min Gab, Geng Xueqing, Lee Sang Yeol, Mackey David

摘要

Plant disease resistance (R) proteins recognize potential pathogens expressing corresponding avirulence (Avr) proteins through 'gene-for-gene' interactions. RPM1 is an Arabidopsis R-protein that triggers a robust defense response upon recognizing the Pseudomonas syringae effector AvrRpm1. Avr-proteins of phytopathogenic bacteria include type III effector proteins that are often capable of enhancing virulence when not recognized by an R-protein. In rpm1 plants, AvrRpm1 suppresses basal defenses induced by microbe-associated molecular patterns. Here, we show that expression of AvrRpm1 in rpm1 plants induced PR-1, a classical defense marker, and symptoms including chlorosis and necrosis. PR-1 expression and symptoms were reduced in plants with mutations in defense signaling genes (pad4, sid2, npr1, rar1, and ndr1) and were strongly reduced in rpm1 rps2 plants, indicating that AvrRpm1 elicits defense signaling through the Arabidopsis R-protein, RPS2. Bacteria expressing AvrRpm1 grew more on rpm1 rps2 than on rpm1 plants. Thus, independent of its classical 'gene-for-gene' activation of RPM1, AvrRpm1 also induces functionally relevant defenses that are dependent on RPS2. Finally, AvrRpm1 suppressed host defenses and promoted the growth of type III secretion mutant bacteria equally well in rps2 and RPS2 plants, indicating that virulence activity of over-expressed AvrRpm1 predominates over defenses induced by weak activation of RPS2.

文献信息
期刊
The Plant journal : for cell and molecular biology
期刊简称
Plant J
发表日期
2009-02-27
收录日期
2009-02-17
更新日期
2009-02-17
语言
英语
国家/地区
England
NLM ID
9207397
分析服务
分析服务

联系地址

山东省济南市章丘区文博路2号

齐鲁师范学院 genelibs生信实验室

山东省济南市高新区舜华路750号

大学科技园北区F座4单元2楼

电话: 0531-88819269

微信公众号

关注微信订阅号,实时查看信息,关注医学生物学动态。


商务邮箱

E-mail: [email protected]