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The metabolite methylglyoxal-mediated gene expression is associated with histone methylglyoxalation

ABSTRACT: The metabolite methylglyoxal-mediated gene expression is associated with histone methylglyoxalation

PROVIDER: PRJNA511620 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8367730.fastq.gz	Fastqsanger.gz
	SRR8367740.fastq.gz	Fastqsanger.gz
	SRR8367750.fastq.gz	Fastqsanger.gz
	SRR8367721.fastq.gz	Fastqsanger.gz
	SRR8367731.fastq.gz	Fastqsanger.gz

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The metabolite methylglyoxal-mediated gene expression is associated with histone methylglyoxalation

Project description:RNA-seq analysis of Arabidopsis wild-type, glyI2, 35S::GLYI2 35S::GLYII4 seedlings suggested that MG mediates salt stress responsive gene expression. ChIP-seq analysis of MG-treated Arabidopsis wild-type seedlings with anti-MMP and anti-H3K4MG suggested that MG-mediated gene expression is associated with histone methylglyoxalation.

2021-01-05 | GSE124328 | GEO

The metabolite methylglyoxal-mediated gene expression is associated with histone methylglyoxalation.

Project description:Methylglyoxal (MG) is a byproduct of glycolysis that functions in diverse mammalian developmental processes and diseases and in plant responses to various stresses, including salt stress. However, it is unknown whether MG-regulated gene expression is associated with an epigenetic modification. Here we report that MG methylglyoxalates H3 including H3K4 and increases chromatin accessibility, consistent with the result that H3 methylglyoxalation positively correlates with gene expression. Salt stress also increases H3 methylglyoxalation at salt stress responsive genes correlated to their higher expression. Following exposure to salt stress, salt stress responsive genes were expressed at higher levels in the Arabidopsis glyI2 mutant than in wild-type plants, but at lower levels in 35S::GLYI2 35S::GLYII4 plants, consistent with the higher and lower MG accumulation and H3 methylglyoxalation of target genes in glyI2 and 35S::GLYI2 35S::GLYII4, respectively. Further, ABI3 and MYC2, regulators of salt stress responsive genes, affect the distribution of H3 methylglyoxalation at salt stress responsive genes. Thus, MG functions as a histone-modifying group associated with gene expression that links glucose metabolism and epigenetic regulation.

| S-EPMC7913762 | biostudies-literature

The Glycolytic Metabolite Methylglyoxal Covalently Inactivates the NLRP3 Inflammasome.

Project description:Mass Spectrometry data showing MICA crosslinking of NLRP3 Pyrin cysteines and arginines induced by methylglyoxal (MGO)

2024-08-01 | MSV000095503 | MassIVE

Hypoxia-mediated regulation of histone demethylases affects angiogenesis associated functions in endothelial cells

Project description:Hypoxia-mediated regulation of histone demethylases affects angiogenesis associated functions in endothelial cells

| PRJNA586868 | ENA

ChIP-chip by array of E. coli MG1655 to analyzed the genome-wide redistribution of RNA polymerase upon methylglyoxal stress

Project description:We have analyzed the genome-wide redistribution of RNA polymerase in E.coli upon methylglyoxal stress. Herefore, we have used ChIP-chip against the beta subunit of RNA polymerase and we have assessed changes in RNA polymerase distribution upon sub-lethal and lethal concentrations of methylglyoxal.

2011-12-15 | E-MTAB-100 | biostudies-arrayexpress

Microarray expression of kidney cortex in adult male rats treated with methylglyoxal vs. controls

Project description:In our study, we investigated the effect of methylglyoxal on metabolic, transcriptomic, metabolomic and proteomic profiles in the context of the development of kidney impairment in an experimental model of metabolic syndrome. Dicarbonyl stress was induced in experimental group by intragastrical administration of methylglyoxal (3x/ week in dose 0.5 mg/kg b.wt.for 4 weeks) in a strain of hereditary hypertriglyceridaemic rats (HHTg). Transcriptome assessment in kidney cortex was performed in 8 male adult rats of experimental group and compared to that of 6 age- and sex- matched rats of control group.

2020-02-08 | E-MTAB-7690 | biostudies-arrayexpress

Chemical Modulation of Glycolysis Regulates the KEAP1-NRF2 Pathway Through a Metabolite-Induced Posttranslational Modification

Project description:Glycolysis is a master regulator of cellular energy, synthesis and redox regulation, however the mechanisms that underlie the responses to and regulation of changing glucose metabolism are incompletely understood. The NRF2-antioxidant response element (ARE) pathway serves as a central regulator of cellular stress by sensing and eliminating 2 chemically reactive species in the cell. A phenotypic high-throughput chemical screen for novel activators of NRF2 signaling identified an inhibitor of the glycolytic enzyme PGK1. Metabolomic and proteomic profiling experiments revealed that inhibition of PGK1 results in the accumulation of central glycolytic intermediates, as well as the reactive dicarbonyl metabolite methylglyoxal (MGx). MGx selectively modifies reactive residues on KEAP1, resulting in the formation of a covalent KEAP1 homodimer, accumulation of NRF2 and activation of the NRF2 transcriptional program. Proteomic and NMR experiments verified that KEAP1 homodimerization is mediated by a novel post-translational modification, termed MICA, formed by the reaction of methylglyoxal with proximal cysteine and arginine residues. The identified PGK1 inhibitor series was found to be efficacious in a NRF2-dependent mouse model of UV-damage, demonstrating that activation of KEAP1- NRF2 signaling through this mechanism is physiologically relevant. Together, these results demonstrate the existence of direct inter-pathway communication between glycolysis and the KEAP1-NRF2 transcriptional program, which is mediated by a reactive metaboliteinduced post-translational modification (rmPTM). In addition, they provide new insight into metabolic regulation of cell stress response, and a potential therapeutic axis for controlling the cytoprotective antioxidant response in numerous human diseases.

2018-10-22 | GSE116642 | GEO

Tricarboxylic Acid Cycle Metabolite-Coordinated Biohydrogels Augment Cranial Bone Regeneration Through Neutrophil-Stimulated MSCs Recruitment and Histone Acetylation-Mediated Osteogenesis

Project description:Tricarboxylic Acid Cycle Metabolite-Coordinated Biohydrogels Augment Cranial Bone Regeneration Through Neutrophil-Stimulated MSCs Recruitment and Histone Acetylation-Mediated Osteogenesis

| PRJNA989116 | ENA

Methylglyoxal modification of TrkB enhances synaptic plasticity in prefrontal cortex and promotes resilience to chronic stress

Project description:Major depressive disorder (MDD) is a severe psychiatric illness that affects about 16 percent of the global population. Despite massive efforts, unravelling the pathophysiology of MDD and developing effective treatments is still a huge challenge. Here, we report a novel therapeutic axis of methylglyoxal (MGO)/tropomyosin receptor kinase B (TrkB) for treating MDD. As an endogenous metabolite, MGO was demonstrated directly binding to the extracellular domain of TrkB, provoking its dimerization and autophosphorylation. This rapidly enhances the expression of brain-derived neurotrophic factor (BDNF) and forms a BDNF-positive feedback loop. Low-dose treatment of MGO effectively promotes the hippocampal neurogenesis and exhibits sustained antidepressant effects in chronic unpredictable mild stress rat models. In addition, the modulation on MGO concentration by overexpression or inhibition of Glyoxalase 1 (GLO1) has been demonstrated associated with depression behaviors in rats. Furthermore, we also identified a natural product luteolin and its derivative lutD as potent inhibitors of GLO1 and explored their precise binding modes. Our findings reveal a novel regulatory mechanism underlying MDD and depict principles for the rational design of new antidepressants targeting GLO1.

2018-09-06 | GSE119482 | GEO

Microarray expression of white adipose tissue in adult male rats treated with methylglyoxal vs. controls

Project description:In our study, we investigated the effect of methylglyoxal on metabolic, transcriptomic, metabolomic and proteomic profiles in the context of metabolic syndrome in an experimental model. Dicarbonyl stress was induced in experimental group by intragastrical administration of methylglyoxal (3x/ week in dose 0.5 mg/kg b.wt.for 4 weeks) in a strain of hereditary hypertriglyceridaemic rats (HHTg). Transcriptome assessment in white adipose tissue was performed in 7 male adult rats of experimental group and compared to that of 6 age- and sex- matched rats of control group.

2021-04-06 | E-MTAB-9013 | biostudies-arrayexpress

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