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The processed C-terminus of avrrps4 effector suppresses plant immunity via targeting multiple WRKYs

Journal of Integrative Plant Biology 2024年第8期66卷 1769-1787页

作者： Quang-Minh Nguyen Arya Bagus Boedi Iswanto Hobin Kang Jiyun Moon Kieu Anh Thi Phan Geon Hui Son Mi Chung Suh Eui-Hwan Chung Walter Gassmann Sang Hee Kim Division of Applied Life Science(BK21 Four Program) Plant Molecular Biology and Biotechnology Research CenterGyeongsang National UniversityJinju 52828Korea Department of Life Science Sogang UniversitySeoul 04107Korea Department of Plant Biotechnology Korea UniversitySeoul 02841Korea Division of Plant Science and Technology Christopher S.Bond Life Sciences Center and Interdisciplinary Plant GroupUniversity of MissouriColumbiaMissouri 65211USA Division of Life Science and Research Institute of Molecular Alchemy Gyeongsang National UniversityJinju 52828Korea

Pathogens generate and secrete effector proteins to the host plant cells during pathogenesis to promote virulence and *** the plant carries resistance(R)proteins that recognize pathogen effectors,effector-triggered immunity(ETI)is activated,resulting in a robust immune response and hypersensitive response(HR).The bipartite effector avrrps4 from Pseudomonas syringae *** has been well studied in terms of avirulence *** planta,avrrps4 is processed into two *** Cterminal fragment of avrrps4(avrrps4^(C))induces HR in turnip and is recognized by the paired resistance proteins AtRRS1/AtRPS4 in ***,we show that avrrps4^(C)targets a group of Arabidopsis WRKY,including WRKY46,WRKY53,WRKY54,and WRKY70,to induce its virulence ***,avrrps4^(C)suppresses the general binding and transcriptional activities of immune-positive regulator WRKY54 and WRKY54-mediated ***4^(C)interferes with WRKY54's binding activity to target gene SARD1 in vitro,suggesting WRKY54 is sequestered from the SARD1 promoter by avrrps4^(C).Through the interaction of Avr Rps4^(C)with four WRKYs,avrrps4 enhances the formation of homo-/heterotypic complexes of four WRKYs and sequesters them in the cytoplasm,thus inhibiting their function in plant ***,our results provide a detailed virulence mechanism of avrrps4 through its C-terminus.

关键词： avrrps4 bacterial effector effector-triggered immunity immune response suppression transcription factor WRKY

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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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