Oryza sativa
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB12353 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR319689_1.fastq.gz | Fastqsanger.gz | |||
| DRR319689_2.fastq.gz | Fastqsanger.gz | |||
| DRR319690_1.fastq.gz | Fastqsanger.gz | |||
| DRR319690_2.fastq.gz | Fastqsanger.gz | |||
| DRR319691_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 16 |
Similar Datasets
Project description:A genetically linked pair of NLR immune receptors show contrasting patterns of evolution
| PRJDB12891 | ENA
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:Characterization of NWD1; a novel NLR-related protein and further correlate it as a putative Prostate Cancer marker. NLRs (NACHT and Leucine Rich Repeat domain containing proteins) constitute a major subfamily of innate immunity proteins mostly acting as cytosolic pattern recognition receptors (PRRs), involved in the detection of cytoplasmic pathogen-associated molecular patterns (PAMPs) and endogenous danger signals. The recognition of the signals initiates a variety of host defense pathways through the activation of NF-kappaB, stress kinases, interferon response factors (IRFs) and/or inflammatory caspases. Despite the importance in host immune response, deregulation on NLR activities has been described in a variety of maladies, including chronic inflammation and cancer predisposition. For instance, NOD1 was one of the first NLR members shown to possibly play a role in tumorigenesis, since NOD1 stimulation induces apoptosis in MCF-7 breast carcinoma cells, and NOD1-/- MCF-7 cells generate larger tumors after injection in SCID mice. Mice deficient in NLR member NLRP3, and/or its interacting partners ASC or caspase-1, are also shown to be more susceptible to colitis-associated cancer (CAC). Polymorphisms along NLR genes NOD1 and NOD2 have also been correlated with altered cancer risk. NOD1 SNPs have been associated with gastric cancer, lymphoma, ovarian, prostate, and lung cancer due to the recognition of H. pylori (etiologic agent in gastric cancer and MALT lymphoma), C. trachomatis (putative etiologic agent in ovarian cancer), P. acnes (possible causative agent in PCa) and C. pneumonia (plausible etiological agent in lung cancer) as NOD1 ligands. Particularly, NOD1 and NOD2 have been shown to be fully operative in prostate epithelial cells and, in cooperation with TLRs, may elicit immune response during PCa progression.
2014-03-07 | GSE53115 | GEO
Project description:Characterization of NWD1; a novel NLR-related protein and further correlate it as a putative Prostate Cancer marker. NLRs (NACHT and Leucine Rich Repeat domain containing proteins) constitute a major subfamily of innate immunity proteins mostly acting as cytosolic pattern recognition receptors (PRRs), involved in the detection of cytoplasmic pathogen-associated molecular patterns (PAMPs) and endogenous danger signals. The recognition of the signals initiates a variety of host defense pathways through the activation of NF-kappaB, stress kinases, interferon response factors (IRFs) and/or inflammatory caspases. Despite the importance in host immune response, deregulation on NLR activities has been described in a variety of maladies, including chronic inflammation and cancer predisposition. For instance, NOD1 was one of the first NLR members shown to possibly play a role in tumorigenesis, since NOD1 stimulation induces apoptosis in MCF-7 breast carcinoma cells, and NOD1-/- MCF-7 cells generate larger tumors after injection in SCID mice. Mice deficient in NLR member NLRP3, and/or its interacting partners ASC or caspase-1, are also shown to be more susceptible to colitis-associated cancer (CAC). Polymorphisms along NLR genes NOD1 and NOD2 have also been correlated with altered cancer risk. NOD1 SNPs have been associated with gastric cancer, lymphoma, ovarian, prostate, and lung cancer due to the recognition of H. pylori (etiologic agent in gastric cancer and MALT lymphoma), C. trachomatis (putative etiologic agent in ovarian cancer), P. acnes (possible causative agent in PCa) and C. pneumonia (plausible etiological agent in lung cancer) as NOD1 ligands. Particularly, NOD1 and NOD2 have been shown to be fully operative in prostate epithelial cells and, in cooperation with TLRs, may elicit immune response during PCa progression. To access a tissue-specific gene expression profile for NWD1, quantitative PCR analysis was performed using a normalized cDNA panel derived from 48 human tissues (TissueScan Tissue qPCR Array, Origene). Two apparently independent expression patterns were detected, respectively related to neurological related organs (brain, pituitary and retina) and male reproductive system (prostate, epididymis and testis), where the highest mRNA levels was observed in prostate tissue. Results were confirmed using a second set of NWD1-specific qPCR primers (data not shown). Moreover, a similar expression pattern was virtually observed using the SAGE database from the Cancer Genome Anatomy Project (CGAP) of the National Cancer Institute (not shown). Comparative gene expression microarray data was analyzed systematically by Ingenuity Pathway Analysis (IPA) to set up potential networks based on NWD1 regulated genes. The eventual participation of NWD1 in signaling transduction pathways was further examined by microarray analysis (Human WG-6v3 Expression BeadChip, Illumina) comparing the expression profile of PPC-1 cells lacking NWD1 expression (sh184 & sh3922) versus control cells (shGFP). According to the differential expression profile that was generated and analyzed by the Ingenuity PathwaysTM software (IPA version 7.1, Ingenuity Systems), NWD1 is presumably associated with biological networks related, for instance, to tissue morphology, organogenesis, cancer and neurological diseases .
2014-03-07 | E-GEOD-53115 | biostudies-arrayexpress
Project description:Crop breeding aims to balance disease resistance with yield; however, single resistance (R) genes can lead to resistance breakdown, and R gene pyramiding may affect growth fitness. Here we report that the rice Pigm locus contains a cluster of genes encoding nucleotide-binding leucine-rich repeat (NLR) receptors that confer durable resistance to the fungus Magnaporthe oryzae without yield penalty. Among these NLR receptors, PigmR confers broad-spectrum resistance, whereas PigmS competitively attenuates PigmR homodimerization to suppress resistance. PigmS expression, and thus PigmR-mediated resistance, are subjected to tight epigenetic regulation. PigmS increases seed production to counteract the yield cost induced by PigmR Therefore, our study reveals a mechanism balancing high disease resistance and yield through epigenetic regulation of paired antagonistic NLR receptors, providing a tool to develop elite crop varieties.
2017-06-15 | GSE83522 | GEO
Project description:Inflammation and immunity play a causal role in the pathogenesis of pulmonary vascular remodeling and pulmonary arterial hypertension (PAH). However, the pathways and mechanisms by which inflammation and immunity contribute to pulmonary vascular remodeling remain unknown. RNA sequencing was used to analyze the transcriptome in control and rats injected with monocrotaline (MCT) for 1, 2, 3 and 4 weeks. Using the transcriptional profiling of MCT-induced PAH coupled with bioinformatics analysis, we clustered the differentially expressed genes (DEGs) and chose the increased expression patterns associated with inflammatory and immune response. We found the enrichment of Toll-like receptor (TLR) and NOD-like receptor (NLR) pathways and identified NF-κB-mediated inflammatory and immune profiling in MCT-induced PAH. Pathway-based data integration and visualization showed the dysregulated TLR and NLR pathways, including increased expression of TLR2 and NLRP3, and their downstream molecules. Further analysis revealed that the activation of TLR and NLR pathways was associated with upregulation of damage-associated molecular patterns (DAMPs) and RIPK3-mediated necroptosis was involved in the generation of DAMPs in MCT-induced PAH. Collectively, we identify RIPK3-mediated necroptosis and its triggered TLR and NLR pathways in the progression of pulmonary vascular remodeling, thus, providing novel insights into the mechanisms underlying inflammation and immunity in the pathogenesis of PAH.
2020-05-02 | GSE149713 | GEO
Project description:Daghestan, with its exceptional combination of linguistic, geographic, and cultural diversity, presents an excellent natural laboratory for tracking the influence of demographic processes on patterns of genetic variation. This study was designed to investigate the co-evolution of genes and languages, comparing and contrasting patterns of linguistic, genetic and geographic variation among Daghestani populations.
2020-01-04 | GSE93106 | GEO
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
Project description:Nucleotide-binding site leucine-rich repeat (NLR) receptors perceive pathogen effectors and trigger plant immunity. However, the mechanisms underlying NLR-triggered defense responses remain obscure. The recently discovered Pigm locus in rice encodes a cluster of NLRs, including PigmR, which confers broad-spectrum resistance to blast fungus. Here, we identify PIBP1 (PigmR-INTERACTING and BLAST RESISTANCE PROTEIN 1), an RRM (RNA-recognition motif) protein that specifically interacts with PigmR and other similar NLRs to trigger blast resistance. PigmR-promoted nuclear accumulation of PIBP1 ensures full blast resistance. We find that PIBP1 and a homolog, Os06 g02240, bind DNA and function as unconventional transcription factors at the promoters of the defense genes OsWAK14 and OsPAL1, activating their expression. Knockout of PIBP1 and Os06 g02240 greatly attenuated blast resistance. Collectively, our study discovers previously unappreciated RRM transcription factors that directly interact with NLRs to activate plant defense, establishing a direct link between transcriptional activation of immune responses with NLR-mediated pathogen perception.
2019-08-04 | GSE118352 | GEO