A glycolytic enzyme enoalse negatively regulates plant immunity by repressing intracellular immune receptor NLR genes
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ABSTRACT:
PROVIDER: PRJNA657243 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12454521.fastq.gz | Fastqsanger.gz | |||
| SRR12454522.fastq.gz | Fastqsanger.gz | |||
| SRR12454523.fastq.gz | Fastqsanger.gz | |||
| SRR12454524.fastq.gz | Fastqsanger.gz | |||
| SRR12454525.fastq.gz | Fastqsanger.gz |
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2017-07-24 | PXD006686 | Pride
Project description:Metabolic fluxes may be regulated "hierarchically," e.g., by changes of gene expression that adjust enzyme capacities (V(max)) and/or "metabolically" by interactions of enzymes with substrates, products, or allosteric effectors. In the present study, a method is developed to dissect the hierarchical regulation into contributions by transcription, translation, protein degradation, and posttranslational modification. The method was applied to the regulation of fluxes through individual glycolytic enzymes when the yeast Saccharomyces cerevisiae was confronted with the absence of oxygen and the presence of benzoic acid depleting its ATP. Metabolic regulation largely contributed to the approximately 10-fold change in flux through the glycolytic enzymes. This contribution varied from 50 to 80%, depending on the glycolytic step and the cultivation condition tested. Within the 50-20% hierarchical regulation of fluxes, transcription played a minor role, whereas regulation of protein synthesis or degradation was the most important. These also contributed to 75-100% of the regulation of protein levels. Experiment Overall Design: To quantify the regulation of the Vmax values and the fluxes at the different levels of gene expression, we measured how the fluxes through the glycolytic enzymes, the Vmax values, and the concentrations of these enzymes and their corresponding mRNA concentrations change when yeast is exposed to aerobic and anaerobic (with and without challenges.
2008-06-16 | E-GEOD-9232 | biostudies-arrayexpress
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2014-03-07 | E-GEOD-53115 | biostudies-arrayexpress
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:Plant immune responses need to be tightly controlled for growth-defense balance. The mechanism underlying this tight control is not fully understood. Here we identify epigenetic regulation of nucleotide-binding leucine rich repeat or Nod-Like Receptor (NLR) genes as an important mechanism for immune responses. Through a sensitized genetic screen and molecular studies, we identified and characterized HOS15 and its associated protein HDA9 as negative regulators of immunity and NLR gene expression. The loss-of-function of HOS15 or HDA9 confers enhanced resistance to pathogen infection accompanied with increased expression of one-third of the 207 NLR genes in Arabidopsis thaliana. HOS15 and HDA9 are physically associated with some of these NLR genes and repress their expression likely through reducing the acetylation of H3K9 at these loci. In addition, these NLR genes are repressed by HOS15 under both pathogenic and nonpathogenic conditions but by HDA9 only under infection condition. Together, this study uncovers a previously uncharacterized histone deacetylase complex in plant immunity and highlights the importance of epigenetic regulation of NLR genes in modulating growth-defense balance.
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2021-04-06 | PXD021301 | Pride