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

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Molecular Plant 2018年第8期11卷 1053-1066页

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

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.

关键词： nlr receptor stress hormone network Pseudomonas syringae AvrRps4 RRS1/RPS4 coi1

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EDS1 modules as two‑tiered receptor complexes for TIR‑catalyzed signaling molecules to activate plant immunity

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Stress Biology 2022年第1期2卷 324-327页

作者： Jia Li Xiaorong Tao The Key Laboratory of Plant Immunity Department of Plant PathologyNanjing Agricultural UniversityNanjing 210095People’s Republic of China

Plant intracellular nucleotide-binding leucine-rich repeat(nlr)receptors with an N-terminal Toll/Interleukin-1 recep-tor(TIR)domain detect pathogen effectors to produce TIR-catalyzed signaling molecules for activation of plant *** immune signaling by TIR-containing nlr(TNL)proteins converges on Enhanced Disease Suscepti-bility 1(EDS1)and its direct partners Phytoalexin Deficient 4(PAD4)or Senescence-Associated Gene 101(SAG101).TNL signaling also require helper nlrs N requirement gene 1(NRG1)and activated disease resistance 1(ADR1).In two recent remarkable papers published in Science,the authors show that the TIR-containing proteins catalyze and produce two types of signaling molecules,ADPr-ATP/diADPR and pRib-AMP/***,they demonstrate that EDS1-SAG101 and EDS1-PAD4 modules are the receptor complexes for ADPr-ATP/diADPRp and Rib-AMP/ADP,respec-tively,which allosterically promote EDS1-SAG101 interaction with NRG1 and EDS1-PAD4 interaction with ***,two different small molecules catalyzed by TIR-containing proteins selectively activate the downstream two distinct branches of EDS1-mediated immune *** breakthrough studies significantly advance our understanding of TNL downstream signaling pathway.

关键词： nlr receptor Toll/Interleukin-1 receptor domain EDS1 PAD4 SAG101 Signaling molecule Plant immunity

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