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Pad4 vs. pad4 est1b

ABSTRACT: This experiment was designed to identify transcripts which are changed in plants deficient for evolutionary conserved EST1B gene. A mutation in est1b leads to a constitutive up-regulation of a PAD4-dependent pathogen response pathway. To eliminate secondary effects of the constitutive pathogen response in est1b mutants we will analyze transcriptoms in plants in which lack PAD4. Keywords: Expression profilling by array

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE18979 | GEO | 2009/11/18

SECONDARY ACCESSION(S): PRJNA121147

REPOSITORIES: GEO

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pad4 vs. pad4 est1b

Project description:This experiment was designed to identify transcripts which are changed in plants deficient for evolutionary conserved EST1B gene. A mutation in est1b leads to a constitutive up-regulation of a PAD4-dependent pathogen response pathway. To eliminate secondary effects of the constitutive pathogen response in est1b mutants we will analyze transcriptoms in plants in which lack PAD4. Keywords: Expression profilling by array 6 samples were used in this experiment

2009-11-17 | E-GEOD-18979 | biostudies-arrayexpress

Study of primary transcriptional changes induced by EDS1/PAD4 in Arabidopsis using an estradiol-inducible system

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

Comparative analysis of PAD4 and SAG101 interactors upon activation of NLR immunity in Arabidopsis thaliana

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

The EDS1-PAD4-ADR1 node mediates Arabidopsis pattern-triggered immunity

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

Cavity surface residues of PAD4 and SAG101 contribute to EDS1 dimer signaling specificity in plant immunity

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

Genes affected by PAD4 deficiency in LSK cells obtained from mouse bone marrow.

Project description:We found PAD4, which is one of the transcriptional co-regulator by histone modification, was highly expressed in lineage-, Sca-1+, c-kit+ (termed as LSK) cells of mouse bone marrow. To find the target genes which are regulated by PAD4 in LSK cells, we analyzed gene expression in PAD4-deficient mouse as compared with wild-type mouse. Gene expression in wild-type and PAD4-deficient LSK cells

2013-06-01 | E-GEOD-45482 | biostudies-arrayexpress

Genes affected by PAD4 deficiency in LSK cells obtained from mouse bone marrow.

2013-06-01 | GSE45482 | GEO

Time-course RNA-seq analysis of the barley MLA1 immune receptor-mediated response to barley powdery mildew fungus Bgh in Arabidopsis thaliana

Project description:We report that an intracellular NLR immune receptor from monocotyledonous barley is fully functional in dicotyledonous Arabidopsis thaliana. In contrast to common belief in plant NLR biology, this implies ~150 million years of evolutionary conservation of the underlying immune mechanism. This also suggests a conserved translocation mechanism for pathogen effectors in flowering plants. The deduced connectivity of the NLR to bifurcated signaling pathways likely confers increased robustness against pathogen interception, which could have contributed to the evolutionary preservation of the immune mechanism. RNA-seq experiments in Arabidopsis detected sustained expression of a single major MLA1-dependent gene cluster. 3 biological replicates per condition. The Arabidopsis plants without (pps) or with (B12) the MLA1-HA construct in a pen2 pad4 sag101 background were challenged with either the Bgh isolate K1 expressing the cognate AVRA1 effector for MLA1 or the Bgh isolate A6 expressing other AVRA effectors. Samples were collected at 6, 12, 18, 24 hours post inoculation (hpi) of Bgh.

2012-11-22 | E-GEOD-39463 | biostudies-arrayexpress

Transcription profiling of Arabidopsis leading to the identification of novel components in the EDS1/PAD4-regulated defence pathwayabidopsis-Pst-eds1-pad4

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

PAD4 controls tumor immunity via restraining the MHC-II machinery in macrophages

Project description:Tumor-associated macrophages (TAMs) shape tumor immunity and therapeutic efficacy. However, it is poorly understood if and how post-translational modifications (PTMs) intrinsically affect the phenotype and function of TAMs. Here, we found that peptidylarginine deiminase 4 (PAD4) manifested the highest expression among common PTM enzymes in TAMs and negatively correlated to clinical response to immune checkpoint blockade (ICB). Genetic and pharmacological inhibition of PAD4 in macrophages prevented tumor progression in tumor-bearing mouse models, accompanied by an increase in macrophage MHC-II expression and T-cell effector function. Mechanistically, PAD4 citrullinated STAT1 at arginine 121 (R121), thereby promoting the interaction between STAT1 and PIAS1; and the loss of PAD4 abolished this interaction, ablating the inhibitory role of PIAS1 in the expression of MHC-II machinery in macrophages and enhancing T-cell activation. Thus, the PAD4-STAT1-PIAS1 axis is a previously unknown intrinsic immune restriction mechanism in macrophages and may serve as a cancer immunotherapy target.

2024-05-22 | PXD049188 | Pride

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