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Excess S-Adenosylmethionine inhibits methylation via catabolism to adenine

ABSTRACT: Excess S-Adenosylmethionine inhibits methylation via catabolism to adenine

PROVIDER: PRJNA764914 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15992555_1.fastq.gz	Fastqsanger.gz
	SRR15992555_2.fastq.gz	Fastqsanger.gz
	SRR15992556_1.fastq.gz	Fastqsanger.gz
	SRR15992556_2.fastq.gz	Fastqsanger.gz
	SRR15992557_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Excess S-Adenosylmethionine inhibits methylation via catabolism to adenine

Project description:Mouse embryonic fibroblasts were treated with 1mM SAM, 1mM adenine or 10microM, and transcriptome signatures were compared to untreated cells.

2021-09-23 | GSE184525 | GEO

Increased Neanderthal ancestry in genomic regions associated with lipid catabolism in contemporary Europeans

Project description:While Neanderthals are extinct, fragments of their genome still persist in the genomes of contemporary humans. Here, we show that such Neanderthal-like sequences are not distributed randomly in contemporary human genomes. Specifically, while genome-wide frequency of Neanderthal-like sites is close to 6% in all out-of-Africa populations, genes involved in lipid catabolism contain large excess Neanderthal-like sequences in Europeans (24.3%), but not in Asians (12.4%). While lipid catabolism cannot be assayed in Neanderthals, we took advantage of genetic divergence between human populations, chimpanzees and Neanderthals to predict metabolic divergence expected from the observed excess of Neanderthal gene flow into Europeans. We confirmed predicted changes in lipid catabolism using hydrophobic metabolome measurements in the brain tissue and further linked these metabolic changes to gene expression divergence. 14 human and 6 chimpanzee samples were sequenced.

2014-03-31 | E-GEOD-45263 | biostudies-arrayexpress

Increased Neanderthal ancestry in genomic regions associated with lipid catabolism in contemporary Europeans

2014-03-31 | GSE45263 | GEO

S-Adenosylmethionine treatment diminishes the proliferation of castration- resistant prostate cancer cells by modulating the expression of miRNAs

Project description:AdoMet (S-adenosylmethionine) inhibits cancer cell proliferation and migration via epigenetic alterations. The aim of this study was to investigate whether AdoMet may cause alterations in miRNA expression profiles important for the initiation and progression of prostate cancer. PC-3 cells were treated with AdoMet prior to miRNA sequencing. 17 differentially expressed miRNAs were detected. Target gene prediction was performed by means of databases. Results were aligned to transcriptomic data. Bioinformatic analysis revealed upregulation of anticancerogenic genes, downregulation of cancerogenic-related processes and pathways. Knocking down hsa-miR-192-5p in PC-3 cells resulted in downregulation of cancer cell proliferation, thus confirming these results.

2024-09-10 | E-MTAB-14388 | biostudies-arrayexpress

Adenine effect on Enterohemorraghic E.coli

Project description:Previous experiments have shown that E. feacalis increases EHEC virulence by secreting adenine, this RNAseq aims to understand the molecular mechanism underlaying adenine role on EHEC

2024-05-01 | GSE244178 | GEO

S-adenosylmethionine decarboxylase-dependent gene expression in planktonic Bacillus subtilis NCIB3610

Project description:The polyamine spermidine is not required for normal planktonic growth of Bacillus subtilis but is essential for robust biofilm formation. In a spermidine-deficient mutant of B. subtilis, the structural analogue norspermidine but not homospermidine restored biofilm formation. Intracellular biosynthesis of another spermidine analogue aminopropylcadaverine from exogenously supplied homoagmatine also restored biofilm formation. The differential ability of C-methylated spermidine analogues to replace the function of spermidine in biofilm formation indicated that the aminopropyl side of spermidine is more sensitive to C-methylation. Together, these data indicate that the aminopropyl side of spermidine is essential for its function in biofilm formation, and that the length and symmetry of the molecule is not critical. Transcriptomic analysis of a spermidine-depleted speD mutant of B. subtilis uncovered a nitrogen, methionine and S-adenosylmethionine sufficiency response, resulting in repression of gene expression related to purine catabolism, methionine and S-adenosylmethionine biosynthesis, methionine salvage, and there were indications that membrane status was altered. Consistent with the requirement for spermidine in biofilm formation, expression of the operons for production of the exopolysaccharide and TasA protein components of the biofilm matrix was reduced, as was expression of regulator SinR antagonist slrR. Single-cell analysis indicated that the effect of spermidine depletion was to decrease the number of cells expressing the biofilm matrix operons. Deletion of sinR or ectopic expression of slrR in the spermidine-deficient ΔspeD background restored biofilm formation, indicating that spermidine is required to promote expression of the biofilm regulator slrR.

2017-03-24 | GSE96942 | GEO

Transcriptome analysis of adenine-treated murine microglial cells

Project description:In previous study, we demonstrated adenine-induced cell signaling on anti-inflammation in BV2 cells. To investigate the changes of transcriptome mediated by adenine, we used microarrays to compare the difference in expression levels.

2017-08-01 | GSE84217 | GEO

Loss of mitochondrial proline catabolism depletes FAD, impairing sperm function, and male reproductive advantage

Project description:Exposure to environmental stress has a clinically established influence on male reproductive health, but the impact of normal cellular metabolism on sperm quality and function is less well-defined. Here we show that homeostatic changes in mitochondrial dynamics driven by defective mitochondrial proline catabolism result in pleiotropic consequences on sperm quality and competitive fitness. Disruption of alh-6, which converts 1-pyrroline-5-carboxylate (P5C) to glutamate, results in P5C accumulation that drives oxidative stress, activation of the cytoprotective transcription factor SKN-1, and a reduction of energy-storing flavin adenine dinucleotide (FAD) levels. These molecular changes lead to premature male reproductive senescence by reducing sperm quality. These sperm-specific defects are suppressed by abating P5C metabolism, by treatment with antioxidants to combat reactive oxygen species (ROS), or by feeding diets that restore FAD levels. Our results define a role for mitochondrial proline catabolism and FAD homeostasis on sperm function and specify strategies to pharmacologically reverse unintended outcomes from SKN-1/Nrf transcriptional activation.

2020-02-17 | GSE121920 | GEO

Treatment of prostate cancer cells with S-adenosylmethionine leads to genomewide alterations of transcription profiles.

Project description:The analysis investigates the impact of methyl donor S-adenosylmethionin on transcription and methylation profiles of prostate carcinoma cells. PC-3 cells (Prostatecarcinoma cells) were treated with 160 micromolar S-adenosylmethionine or vehicle

2015-07-25 | E-GEOD-71303 | biostudies-arrayexpress

Hepatic Phosphatidylcholine Catabolism Driven by PNPLA7 and PNPLA8 Supplies Endogenous Choline to Replenish the Methionine Cycle with Methyl Groups III

Project description:Choline supplies methyl groups for regeneration of methionine and the methyl donor S-adenosylmethionine in the liver. Here we demonstrate that the catabolism of membrane phosphatidylcholine (PC) into water-soluble glycerophosphocholine (GPC) by the phospholipase/lysophospholipase PNPLA8-PNPLA7 axis enables endogenous choline stored in hepatic PC to be utilized in methyl metabolism. PNPLA7-deficient mice show marked decreases in hepatic GPC, choline, and several metabolites related to the methionine cycle, accompanied by various signs of methionine insufficiency including growth retardation, hypoglycemia, hypolipidemia, increased energy consumption, reduced adiposity, increased FGF21, and an altered epigenetic methylation landscape. Moreover, PNPLA8-deficient mice recapitulate most of these phenotypes. In contrast to wild-type mice fed a methionine/choline-deficient diet, both knockout strains display a decreased hepatic triglyceride likely via reductions of lipogenesis and GPC-derived glycerol flux. Collectively, our findings highlight the biological importance of phospholipid catabolism driven by PNPLA8/PNPLA7 in methyl group flux and triglyceride synthesis in the liver.

2022-11-30 | GSE217137 | GEO

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