Arabidopsis thaliana
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA383861 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5467180.fastq.gz | Fastqsanger.gz | |||
| SRR5467190.fastq.gz | Fastqsanger.gz | |||
| SRR5467200.fastq.gz | Fastqsanger.gz | |||
| SRR5467210.fastq.gz | Fastqsanger.gz | |||
| SRR5467220.fastq.gz | Fastqsanger.gz |
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Project description:We observed inhibition of the hypersensitive response (a typical ETI response) by PTI signaling in an Arabidopsis quadruple mutant dde2 ein2 pad4 sid2 (quad). Thus, we designed an experiment to see the interaction between ETI and PTI signaling at the transcriptome level. The Arabidopsis line dde2 ein2 pad4 sid2 Ed-AvrRpt2 (quadAvrRpt2) was used (Ed-AvrRpt2, estradiol-inducible AvrRpt2 transgene). In this plant line, ETI can be elicited by estradiol (Ed) treatment via in planta expression of AvrRpt2. Transcriptome responses to PTI only, ETI only, and PTI+ETI together were recorded.
2017-08-07 | GSE98075 | GEO
Project description:Effector-Triggered Immunity (ETI) and Pattern-Triggered Immunity (PTI) are well-defined modes of plant immunity triggered by recognition of pathogen effector proteins and microbe-associated molecular patterns, respectively. While ETI and PTI network extensively share signaling components, the shared components are used in different ways, resulting in distinct network properties in the model plant Arabidopsis: immunity is highly robust against network perturbations in ETI but relatively sensitive in PTI. However, the molecular mechanism how the shared network leads to the different properties is not known. Here we show that salicylic acid (SA) reponsive genes can respond in the absense of SA during ETI. A 24 DNA microarray study using total RNA from Arabidopsis wildtype Col-0 and sid2-2 mutant infected with Pto hrcC-, Pto EV, Pto AvrRpt2 or water.
2014-07-29 | E-GEOD-40544 | biostudies-arrayexpress
Project description:Effector-Triggered Immunity (ETI) and Pattern-Triggered Immunity (PTI) are well-defined modes of plant immunity triggered by recognition of pathogen effector proteins and microbe-associated molecular patterns, respectively. While ETI and PTI network extensively share signaling components, the shared components are used in different ways, resulting in distinct network properties in the model plant Arabidopsis: immunity is highly robust against network perturbations in ETI but relatively sensitive in PTI. However, the molecular mechanism how the shared network leads to the different properties is not known. Here we show that sustained MAPK activation compensate salicylic acid (SA) signaling. A 12 DNA microarray study using total RNA from Arabidopsis transgenic plants carrying DEX-inducible MKK4DD in Col or sid2-2 background treated with DEX or control.
2014-07-29 | E-GEOD-40547 | biostudies-arrayexpress
Project description:Plants deploy cell surface and intracellular leucine rich-repeat domain (LRR) immune receptors to detect pathogens. LRR receptor kinases (LRR-RKs) and LRR receptor proteins (LRR-RPs) recognise microbe-derived molecules to elicit pattern-triggered immunity (PTI), whereas nucleotide-binding LRR (NLR) proteins detect microbial effectors inside cells to confer effector-triggered immunity (ETI). Although PTI and ETI are initiated in different host cell compartments, they rely on the transcriptional activation of similar sets of genes, suggesting pathway convergence upstream of nuclear events. We report that PTI triggered by Arabidopsis LRR-RP (RLP23) requires signalling-competent dimers of the lipase-like proteins EDS1 and PAD4, and ADR1-family helper NLRs, which are all components of ETI. The cell surface LRR-RK SOBIR1 links RLP23 with EDS1, PAD4 and ADR1 proteins, suggesting formation of constitutive supramolecular complexes containing PTI receptors and transducers at the inner side of the plasma membrane.
2021-07-05 | PXD026120 | Pride
Project description:Effector-Triggered Immunity (ETI) and Pattern-Triggered Immunity (PTI) are well-defined modes of plant immunity triggered by recognition of pathogen effector proteins and microbe-associated molecular patterns, respectively. While ETI and PTI network extensively share signaling components, the shared components are used in different ways, resulting in distinct network properties in the model plant Arabidopsis: immunity is highly robust against network perturbations in ETI but relatively sensitive in PTI. However, the molecular mechanism how the shared network leads to the different properties is not known. Here we show that salicylic acid (SA) reponsive genes can respond in the absense of SA during ETI.
2014-07-29 | GSE40544 | GEO
Project description:Effector-Triggered Immunity (ETI) and Pattern-Triggered Immunity (PTI) are well-defined modes of plant immunity triggered by recognition of pathogen effector proteins and microbe-associated molecular patterns, respectively. While ETI and PTI network extensively share signaling components, the shared components are used in different ways, resulting in distinct network properties in the model plant Arabidopsis: immunity is highly robust against network perturbations in ETI but relatively sensitive in PTI. However, the molecular mechanism how the shared network leads to the different properties is not known. Here we show that sustained MAPK activation compensate salicylic acid (SA) signaling.
2014-07-29 | GSE40547 | GEO
Project description:The plant innate immunity consists of the two interconnected mechanisms, pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). Although much is known about how plants trigger immune responses upon pathogen recognition, the genetic program by which plants avoid an overshoot in pathogen-triggered immune responses remains largely unknown. Here, we discovered a trihelix transcription factor, GT-3a, as an immune-inducible negative regulator of bacterial resistance in Arabidopsis thaliana. Analysis of public RNA-seq data revealed that GT-3a is specifically induced by ETI activation not by PTI activation. Overexpression of GT-3a suppressed resistance against the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 (Pto) and Pto-elicited expression of salicylic acid (SA)-responsive genes. Our results suggest that transcriptional induction of GT-3a circumvents the overshooting of SA-mediated defense responses during ETI.
2024-02-18 | GSE248054 | GEO
Project description:Plants have evolved a two-layered immune system that mainly includes pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) against pathogen attack. PTI and ETI signaling are functionally linked, but also distinct due to specific perceived ligands and activation modes. Unraveling how PTI and ETI coordinate the immune responses against pathogens is crucial for understanding the regulatory mechanisms in plant immunity. To better understand the protein profiling and phosphorylation events during PTI and ETI, we employed integrated whole proteome and phosphoproteome analyses in the tomato-Pst pathosystem with different Pst DC3000 mutants that allow dissection of different layers of immune responses. A total of 225 proteins and 79 phosphopeptides were differentially regulated in tomato leaves during immune responses. Our proteomics results indicate that some overlapping immune responses are triggered by both PTI and ETI-inducing treatment, and ETI response is more robust than PTI response for most proteins. The change patterns of protein abundance and phosphorylation revealed some key regulators involved in Ca2+ signaling, mitogen-activated protein kinase cascades, and reversible protein phosphorylation, ROS and redox homeostasis, direct defense, transcription machinery and protein turnover, cell wall remodeling, hormone biosynthesis, as well as immune molecule accumulation, are modulated during PTI and/or ETI, suggesting their common or specific roles in plant immune responses. However, NAC domain protein and lipid particle serine esterase, two PTI-specific genes from previous transcriptomic work, have not been detected as differentially regulated in our proteomic analysis, and they were proved to be not PTI-specific inducible and therefore cannot be used as PTI-reporters through “overlapping circle” pattern assay. These results provide insights into the fine-tuned regulatory mechanisms between PTI and ETI in-Pst pathosystem, which will springboard further investigations into the sophisticated mechanisms in plant immunity.
2021-11-25 | PXD028240 | Pride
Project description:Plants have a wide variety of ways to defend against pathogens. A commonly used model of the plant immune system divides it into a general response triggered by pathogen associated molecular patterns (PAMPs) and a specific response triggered by effectors. The first type of response is known as PAMP triggered immunity (PTI) and the second as effector-triggered immunity (ETI). We have performed a proteomical analysis of one PTI and two ETI models in potato and compared their effect on protein expression.
2019-10-17 | PXD012576 | Pride
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