Systemic Acquired Resistance: Turning Local Infection into Global Defense

被引：1029

作者：

Fu, Zheng Qing ^{[1
]}

Dong, Xinnian

机构：

[1] Duke Univ, Gordon & Betty Moore Fdn, Howard Hughes Med Inst, Durham, NC 27708 USA

来源：

ANNUAL REVIEW OF PLANT BIOLOGY, VOL 64 | 2013年 / 64卷

基金：

美国国家科学基金会;

关键词：

salicylic acid; PR genes; NPR proteins; mobile signals; WRKY TRANSCRIPTION FACTORS; CONJUGATES AMINO-ACIDS; DNA-BINDING ACTIVITY; SALICYLIC-ACID; DISEASE RESISTANCE; ARABIDOPSIS-THALIANA; GENE-EXPRESSION; PSEUDOMONAS-SYRINGAE; SIGNALING PATHWAYS; MEDIATOR COMPLEX;

D O I：

10.1146/annurev-arplant-042811-105606

中图分类号：

Q94 [植物学];

学科分类号：

071001 ;

摘要：

Systemic acquired resistance (SAR) is an induced immune mechanism in plants. Unlike vertebrate adaptive immunity, SAR is broad spectrum, with no specificity to the initial infection. An avirulent pathogen causing local programmed cell death can induce SAR through generation of mobile signals, accumulation of the defense hormone salicylic acid, and secretion of the antimicrobial PR (pathogenesis-related) proteins. Consequently, the rest of the plant is protected from secondary infection for a period of weeks to months. SAR can even be passed on to progeny through epigenetic regulation. The Arabidopsis NPR1 (non-expresser of PR genes 1) protein is a master regulator of SAR. Recent study has shown that salicylic acid directly binds to the NPR1 adaptor proteins NPR3 and NPR4, regulates their interactions with NPR1, and controls NPR1 protein stability. However, how NPR1 interacts with TGA transcription factors to activate defense gene expression is still not well understood. In addition, redox regulators, the mediator complex, WRKY transcription factors, endoplasmic reticulum-resident proteins, and DNA repair proteins play critical roles in SAR.

引用

页码：839 / 863

页数：25

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