title: ETHYLENE INSENSITIVE3 and ETHYLENE INSENSITIVE3-LIKE1 repress SALICYLIC ACID INDUCTION DEFICIENT2 expression to negatively regulate plant innate immunity in Arabidopsis.
abstract: Pathogen/microbe-associated molecular patterns (PAMPs/MAMPs) trigger plant immunity that forms the first line inducible defenses in plants. The regulatory mechanism of MAMP-triggered immunity, however, is poorly understood. Here, we show that Arabidopsis thaliana transcription factors ETHYLENE INSENSITIVE3 (EIN3) and ETHYLENE INSENSITIVE3-LIKE1 (EIL1), previously known to mediate ethylene signaling, also negatively regulate PAMP-triggered immunity. Plants lacking EIN3 and EIL1 display enhanced PAMP defenses and heightened resistance to Pseudomonas syringae bacteria. Conversely, plants overaccumulating EIN3 are compromised in PAMP defenses and exhibit enhanced disease susceptibility to Pseudomonas syringae. Microarray analysis revealed that EIN3 and EIL1 negatively control PAMP response genes. Further analyses indicated that SALICYLIC ACID INDUCTION DEFICIENT2 (SID2), which encodes isochorismate synthase required for pathogen-induced biosynthesis of salicylic acid (SA), is a key target of EIN3 and EIL1. Consistent with this, the ein3-1 eil1-1 double mutant constitutively accumulates SA in the absence of pathogen attack, and a mutation in SID2 restores normal susceptibility in the ein3 eil1 double mutant. EIN3 can specifically bind SID2 promoter sequence in vitro and in vivo. Taken together, our data provide evidence that EIN3/EIL1 directly target SID2 to downregulate PAMP defenses.
authors.affiliation: School of Agriculture and Biology, Shanghai Jiaotong University, Shanghai 200240, China.
authors.forename: Huamin
authors.initials: H
authors.lastname: Chen
authors.forename: Li
authors.initials: L
authors.lastname: Xue
authors.forename: Satya
authors.initials: S
authors.lastname: Chintamanani
authors.forename: Hugo
authors.initials: H
authors.lastname: Germain
authors.forename: Huiqiong
authors.initials: H
authors.lastname: Lin
authors.forename: Haitao
authors.initials: H
authors.lastname: Cui
authors.forename: Run
authors.initials: R
authors.lastname: Cai
authors.forename: Jianru
authors.initials: J
authors.lastname: Zuo
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Tang
authors.forename: Xin
authors.initials: X
authors.lastname: Li
authors.forename: Hongwei
authors.initials: H
authors.lastname: Guo
authors.forename: Jian-Min
authors.initials: JM
authors.lastname: Zhou
mesh_terms: D017360:Arabidopsis / Q000235:genetics / Q000276:immunology* / Q000378:metabolism* / Q000382:microbiology; D029681:Arabidopsis Proteins / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D047369:Chromatin Immunoprecipitation; D004268:DNA-Binding Proteins; D024202:Electrophoretic Mobility Shift Assay; D018506:Gene Expression Regulation, Plant; D007113:Immunity, Innate / Q000235:genetics / Q000502:physiology*; D015151:Immunoblotting; D019751:Intramolecular Transferases / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D020411:Oligonucleotide Array Sequence Analysis; D030821:Plants, Genetically Modified / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D011401:Promoter Regions, Genetic; D044224:Pseudomonas syringae / Q000472:pathogenicity; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism / Q000502:physiology*
chemical_list: D029681:Arabidopsis Proteins; D004268:DNA-Binding Proteins; C494589:EIL1 protein, Arabidopsis; C106987:EIN3 protein, Arabidopsis; D009687:Nuclear Proteins; D014157:Transcription Factors; D019751:Intramolecular Transferases; C058486:isochorismate synthase