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Control of salicylic acid synthesis and systemic acquired resistance by two members of a plant-specific family of transcription factors
Yaxi Zhanga,b,1, Shaohua Xua,c,1, Pingtao Dinga,b,1, Dongmei Wangd,2, Yu Ti Chengd, Jing Hea, Minghui Gaoa, Fang Xud, Yan Lia, Zhaohai Zhua, Xin Lid, and Yuelin Zhanga,3
aNational Institute of Biological Sciences, Zhongguancun Life Science Park, Beijing 102206, China;
bCollege of Life Sciences, Beijing Normal University, Beijing 100875, China;
cGraduate Program, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China; and
dMichael Smith Laboratories, University of British Columbia, Vancouver, BC , Canada V6T 1Z4
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.
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