Canonical ETI-Dependent and -Independent Pathways Mediate Autoimmunity Caused by Loss of CBP60b Clade Function
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE335760 | GEO | 2026/07/15
REPOSITORIES: GEO
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Project description:Arabidopsis Enhanced Disease Susceptibility 1 (EDS1) and its direct partner Phytoalexin Deficient 4 (PAD4) are required for both basal resistance against virulent pathogens and innate immune responses mediated by all tested TIR (Toll-Interleukin-1 Receptors) type nucleotide-binding/leucine-rich-repeat (NLR) receptors. Using transgenic Arabidopsis plants in Col-0 eds1-2 pad4-1 background conditionally expressing PAD4 and constitutively expressing EDS1 (ED-P4E1), an EDS1/PAD4 immune response can be triggered by estradiol treatment and can induce expression of defense-related genes and lead to enhanced basal resistance. In order to capture primary transcriptional changes in response to EDS1/PAD4, we performed RNA-seq gene expression analysis in ED-P4E1 plants after estradiol or mock treatment at three time points: 6, 12 and 24 h.
2016-09-27 | GSE80585 | GEO
Project description:Arabidopsis pathogen effector-triggered immunity (ETI) is controlled by a family of three lipase-like proteins EDS1, PAD4 and SAG101 and two sub-families of HET-S/LOB-B (HeLo)-domain “helper” NLRs, ADR1s and NRG1s. EDS1-PAD4 dimers cooperate with ADR1s, and EDS1-SAG101 dimers with NRG1s, in two separate defense-promoting modules. EDS1-PAD4-ADR1 and EDS1- SAG101-NRG1 complexes were detected in immune-activated leaf extracts but the molecular determinants for specific complex formation and function remain unknown. EDS1 signaling is mediated by a C-terminal EP domain (EPD) surface surrounding a cavity formed by the heterodimer. Here we investigated whether the EPDs of PAD4 and SAG101 contribute to EDS1 dimer functions. Using a structure-guided approach, we undertook a comprehensive mutational analysis of Arabidopsis PAD4. We identify two conserved residues (Arg314 and Lys380) lining the PAD4 EPD cavity that are essential for EDS1-PAD4 mediated pathogen resistance, but are dispensible for PAD4 mediated restriction of green peach aphid infestation. Positionally equivalent Met304 and Arg373 at the SAG101 EPD cavity are required for EDS1-SAG101 promotion of ETI-related cell death. In a PAD4 and SAG101 interactome analysis of ETI-activated tissues, PAD4R314A and SAG101M304R EPD variants maintain interaction with EDS1 but lose association, respectively, with helper NLRs ADR1-L1 and NRG1.1, and other immune-related proteins. Our data reveal a fundamental contribution of similar but non-identical PAD4 and SAG101 EPD surfaces to specific EDS1 dimer protein interactions and pathogen immunity.
2022-03-17 | PXD029477 | Pride
Project description:Purpose: To understand the autoimmune phenotype in the ka120 mutant and the suppression of ka120 phenotype by the pad4 and ndr1 mutant, we performed the whole genome transcriptome analysis on three-week-old Arabidopsis WT, ka120, ka120 pad4, and ka120 ndr1 plants (the entire rosette was sampled).
2021-02-19 | GSE147682 | GEO
Project description:Intracellular NLR receptors with a central nucleotide-binding domain allow plants to detect specific pathogen-secreted proteins and initiate immune signaling. A family of conserved Enhanced disease susceptibility 1 proteins with a lipase-like and the EP domain transduces the signal from activated NLRs downstream. This family includes EDS1, PAD4 and SAG101 that form mutually exclusive heterodimers EDS1-PAD4 and EDS1-SAG101. Despite sequence similarities, PAD4 and SAG101 control different aspects of NLR immune signaling. More specifically, PAD4 and SAG101 regulate resistance and cell death outputs of the NLR receptor pair RRS1-RPS4, respectively. Also, PAD4 and SAG101 genetically cooperate with distinct downstream signaling NLRs - ADR1 and NRG1. The main aim of this IP-LC/MS project is to assess whether PAD4 and SAG101 form complexes with ADR1 and NRG1 and to gain insight into mechanisms of the genetically established functional links between EDS1 family proteins and downstream signaling NLRs.
2021-04-06 | PXD021301 | Pride
Project description:Expression profiling of wild-type plants and mutants with defects in key components of the defense signaling network was used to model the Arabidopsis network 24 hours after infection by Pseudomonas syringae pv. maculicola strain Psm ES4326. Results using the Affymetrix ATH1 array revealed that expression levels of most pathogen-responsive genes were affected by mutations in coi1, ein2, npr1, pad4, or sid2. These five mutations defined a small number of different expression patterns displayed by the majority of pathogen-responsive genes. P. syringae pv. tomato strain Pst DC3000 elicited a much weaker salicylic acid response than Psm ES4326. Additional mutants were profiled using a custom array. Profiles of pbs3 and ndr1 revealed major effects of these mutations and allowed PBS3 and NDR1 to be placed between the EDS1/PAD4 node and the SA synthesis node in the defense network. Comparison of coi1, dde2, and jar1 profiles showed that many genes were affected by coi1, but very few were affected by dde2 or jar1. Profiles of coi1 plants infected with Psm ES4326 were very similar to those of wild-type plants infected with bacteria unable to produce the phytotoxin coronatine, indicating that essentially all COI1-dependent gene expression changes in this system are caused by coronatine. This experiment consists of three biological replicates. For each genotype, two leaves per plant were pooled from three pots to prepare total RNA.
2008-07-18 | E-GEOD-11009 | biostudies-arrayexpress
Project description:Expression profiling of wild-type plants and mutants with defects in key components of the defense signaling network was used to model the Arabidopsis network 24 hours after infection by Pseudomonas syringae pv. maculicola strain Psm ES4326. Results using the Affymetrix ATH1 array revealed that expression levels of most pathogen-responsive genes were affected by mutations in coi1, ein2, npr1, pad4, or sid2. These five mutations defined a small number of different expression patterns displayed by the majority of pathogen-responsive genes. P. syringae pv. tomato strain Pst DC3000 elicited a much weaker salicylic acid response than Psm ES4326. Additional mutants were profiled using a custom array. Profiles of pbs3 and ndr1 revealed major effects of these mutations and allowed PBS3 and NDR1 to be placed between the EDS1/PAD4 node and the SA synthesis node in the defense network. Comparison of coi1, dde2, and jar1 profiles showed that many genes were affected by coi1, but very few were affected by dde2 or jar1. Profiles of coi1 plants infected with Psm ES4326 were very similar to those of wild-type plants infected with bacteria unable to produce the phytotoxin coronatine, indicating that essentially all COI1-dependent gene expression changes in this system are caused by coronatine.
2008-07-18 | GSE11009 | GEO
Project description:Gene expression profiling leading to the identification of novel components in the EDS1/PAD4-regulated defence pathway
2006-02-15 | E-MEXP-546 | biostudies-arrayexpress
Project description:There is growing evidence that for a comprehensive insight into the function of plant genes it is crucial to assess their functionalities under a wide range of conditions. In this study we examined the role of LESION SIMULATING DISEASE1 (LSD1), ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) and PHYTOALEXIN DEFICIENT4 (PAD4) in the regulation of photosynthesis, water use efficiency (WUE), ROS/hormonal homeostasis and seed yield in Arabidopsis thaliana grown in the laboratory and in the field. We demonstrate that the LSD1 null mutant (lsd1), which is known to exhibit a runaway cell death in non-permissive conditions, proves to be more tolerant to combined drought and high-light stress than the wild type. Moreover, depending on growing conditions, it shows variations in WUE, salicylic acid and hydrogen peroxide concentrations, photosystem II maximum efficiency and in transcription profiles. However, despite these changes, lsd1 demonstrates similar seed yield under all tested conditions. All of these traits depend on EDS1 and PAD4. The differences in the pathways prevailing in the lsd1 in various growing environments are manifested by the significantly smaller number of transcripts deregulated in the field compared to the laboratory, with only 43 commonly regulated genes. Our data indicate that LSD1, EDS1 and PAD4 participate in the regulation of various molecular and physiological processes that influence Arabidopsis fitness. On the basis of these results we emphasize that the function of such important regulators as LSD1, EDS1 and PAD4 should be studied not only under stable laboratory conditions, but also in the environment abounding in multiple stresses. Six genotypes x two conditions experiment including five-week-old WT (Ws), lsd1, pad4, eds1, eds1lsd1, and pad4lsd1 plants grown in laboratory or field conditions, hybridized in two loop-designs (lab and field). Two biological replicates. In total, 2 x 12 samples were hybridized on 24 Arabidopsis Gene Expression microarrays V4 (Agilent, two-color array) including color swap of replicate samples.
2013-02-07 | E-GEOD-24766 | biostudies-arrayexpress
Project description:TIR-type nucleotide-binding leucine-rich repeat domain proteins (TNLs) constitute one major group of immune receptors in dicotyledonous plants. Under normal conditions, TNLs can detect non-self or modified-self within the plant cytoplasm to activate immune signaling characterized by extensive transcriptional reprogramming and efficiently counteracting pathogen infection. At the same time, TNLs, in negative epistatic interaction with a second endogeneous locus or allele are causal for induction of autoimmunity or hybrid necrosis. Both native, pathogen-induced TNL responses and autoimmunity are fully dependent on the plant-specific lipase-like protein EDS1, which is a central integrator for all TNL-mediated responses. EDS1 signals within structurally similar, but spatially distinct complexes with PAD4 and SAG101. We here analyzed stable transgenic lines expressing an EDS1 fusion with enforced nuclear localization. Even in absence of SAG101, nuclear-localized EDS1-PAD4 complexes are fully sufficient to function in basal and effector-triggered immunity. Furthermore, we show that nuclear EDS1, when expressed to high levels, can induce autoimmuity in combination with an RPP1-like gene cluster from ecotype Ler. RPP1-like genes are also implicated in several cases of hybrid necrosis, and we can identify the RPP1 paralog R8 as causal for autoimmunity induction by nuclear EDS1 and a previously characterized, EMS-induced mutation. This highlights the important role of EDS1-family proteins in the nuclear compartment in different immune-like responses.
2017-02-09 | GSE65415 | GEO
Project description:There is growing evidence that for a comprehensive insight into the function of plant genes it is crucial to assess their functionalities under a wide range of conditions. In this study we examined the role of LESION SIMULATING DISEASE1 (LSD1), ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) and PHYTOALEXIN DEFICIENT4 (PAD4) in the regulation of photosynthesis, water use efficiency (WUE), ROS/hormonal homeostasis and seed yield in Arabidopsis thaliana grown in the laboratory and in the field. We demonstrate that the LSD1 null mutant (lsd1), which is known to exhibit a runaway cell death in non-permissive conditions, proves to be more tolerant to combined drought and high-light stress than the wild type. Moreover, depending on growing conditions, it shows variations in WUE, salicylic acid and hydrogen peroxide concentrations, photosystem II maximum efficiency and in transcription profiles. However, despite these changes, lsd1 demonstrates similar seed yield under all tested conditions. All of these traits depend on EDS1 and PAD4. The differences in the pathways prevailing in the lsd1 in various growing environments are manifested by the significantly smaller number of transcripts deregulated in the field compared to the laboratory, with only 43 commonly regulated genes. Our data indicate that LSD1, EDS1 and PAD4 participate in the regulation of various molecular and physiological processes that influence Arabidopsis fitness. On the basis of these results we emphasize that the function of such important regulators as LSD1, EDS1 and PAD4 should be studied not only under stable laboratory conditions, but also in the environment abounding in multiple stresses.
2013-02-07 | GSE24766 | GEO