Antagonism of Transcription Factor MYC2 by EDS1/PAD4 Complexes Bolsters Salicylic Acid Defense in Arabidopsis Effector-Triggered Immunity

作     者：Haitao Cui Jingde Qiu Yue Zhou Deepak D. Bhandari Chunhui Zhao Jaqueline Bautor Jane E. Parker 

作者机构：Department of Plant-Microbe Interactions Max-Planck Institute for Plant Breeding Research Carl-von-Linne Weg 10 50829 Cologne Germany Department of Plant Developmental Biology Max-Planck Institute for Plant Breeding Research 50829 Cologne Germany Key Laboratory of Ministry of Education for Genetics Breeding and Multiple Utilization of Crops Plant Immunity Center Fujian Agriculture University Fuzhou 350002 China These authors contributed equaily to this article. 

出 版 物：《Molecular Plant》 (分子植物（英文版）)

年 卷 期：2018年第11卷第8期

页      面：1053-1066页

核心收录：

学科分类：0710[理学-生物学] 071010[理学-生物化学与分子生物学] 081704[工学-应用化学] 07[理学] 08[工学] 0817[工学-化学工程与技术] 09[农学] 0903[农学-农业资源与环境] 0901[农学-作物学] 0902[农学-园艺学] 0713[理学-生态学] 

基　　金：This work was funded by The Max Planck Society  an Alexander von Hum-boldt Foundation postdoctoral fellowship  and the National Nature Science Foundation of China (Grant 31770277) (HC)  a Chinese Scholarship Council PhD fellowship (CSC) (JQ) and Deutsche Forschungsgemein- schaft SFB 670 grant (JEP  DB) 

主　　题：NLR receptor stress hormone network Pseudomonas syringae AvrRps4 RRS1/RPS4 coi1 

摘      要：In plant immunity, pathogen-activated intracellular nucleotide binding/leucine rich repeat （NLR） receptors mobilize disease resistance pathways, but the downstream signaling mechanisms remain obscure. Enhanced disease susceptibility 1 （EDS1） controls transcriptional reprogramming in resistance triggered by Toll-lnterleukinl-Receptor domain （TIR）-family NLRs （TNLs）. Transcriptional induction of the salicylic acid （SA） hormone defense sector provides one crucial barrier against biotrophic pathogens. Here, we present genetic and molecular evidence that in Arabidopsis an EDS1 complex with its partner PAD4 inhibits MYC2, a master regulator of SA-antagonizing jasmonic acid （JA） hormone pathways. In the TNL immune response, EDSl/PAD4 interference with MYC2 boosts the SA defense sector independently of EDS1-induced SA synthesis, thereby effectively blocking actions of a potent bacterial JA mimic, coronatine （COR）. We show that antagonism of MYC2 occurs after COR has been sensed inside the nucleus but before or coincident with MYC2 binding to a target promoter, pANAC019. The stable interaction of PAD4 with MYC2 in planta is competed by EDS1-PAD4 complexes. However, suppression of MYC2-promoted genes requires EDS1 together with PAD4, pointing to an essential EDS1-PAD4 heterodimer activity in MYC2 inhibition. Taken together, these results uncover an immune receptor signaling circuit that intersects with hormone pathway crosstalk to reduce bacterial pathogen growth.