Control of salicylic acid synthesis and systemic acquired resistance by two members of a plant-specific family of transcription factors

被引:343
作者
Zhang, Yaxi [1 ,2 ]
Xu, Shaohua [1 ,3 ,4 ]
Ding, Pingtao [1 ,2 ]
Wang, Dongmei [5 ]
Cheng, Yu Ti [5 ]
He, Jing [1 ]
Gao, Minghui [1 ]
Xu, Fang [5 ]
Li, Yan [1 ]
Zhu, Zhaohai [1 ]
Li, Xin [5 ]
Zhang, Yuelin [1 ]
机构
[1] Natl Inst Biol Sci, Beijing 102206, Peoples R China
[2] Beijing Normal Univ, Coll Life Sci, Beijing 100875, Peoples R China
[3] Chinese Acad Med Sci, Grad Program, Beijing 100730, Peoples R China
[4] Peking Union Med Coll, Beijing 100730, Peoples R China
[5] Univ British Columbia, Michael Smith Labs, Vancouver, BC V6T 1Z4, Canada
关键词
plant immunity; SAR Deficient 1; Isochorismate Synthase 1; CBP60g; INNATE IMMUNITY; ARABIDOPSIS; INDUCTION; INDUCERS; DISEASE; INOCULATION; EXPRESSION; CUCUMBER; MUTANTS; TOBACCO;
D O I
10.1073/pnas.1005225107
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
Salicylic acid (SA) is a defense hormone required for both local and systemic acquired resistance (SAR) in plants. Pathogen infections induce SA synthesis through up-regulating the expression of Isochorismate Synthase 1 (ICS1), which encodes a key enzyme in SA production. Here we report that both SAR Deficient 1 (SARD1) and CBP60g are key regulators for ICS1 induction and SA synthesis. Whereas knocking out SARD1 compromises basal resistance and SAR, overexpression of SARD1 constitutively activates defense responses. In the sard1-1 cbp60g-1 double mutant, pathogen-induced ICS1 up-regulation and SA synthesis are blocked in both local and systemic leaves, resulting in compromised basal resistance and loss of SAR. Electrophoretic mobility shift assays showed that SARD1 and CBP60g represent a plant-specific family of DNA-binding proteins. Both proteins are recruited to the promoter of ICS1 in response to pathogen infections, suggesting that they control SA synthesis by regulating ICS1 at the transcriptional level.
引用
收藏
页码:18220 / 18225
页数:6
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