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Methionine metabolism shapes T helper cell responses through regulation of epigenetic reprogramming

ABSTRACT: Methionine metabolism shapes T helper cell responses through regulation of epigenetic reprogramming

PROVIDER: PRJNA600853 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10876001.fastq.gz	Fastqsanger.gz
	SRR10876002.fastq.gz	Fastqsanger.gz
	SRR10876003.fastq.gz	Fastqsanger.gz
	SRR10876004.fastq.gz	Fastqsanger.gz
	SRR10876005.fastq.gz	Fastqsanger.gz

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Methionine metabolism shapes T helper cell responses through regulation of epigenetic reprogramming [ChIP-Seq]

Project description:Epigenetic modifications on DNA and histones regulate gene expression by modulating chromatin accessibility to transcription machinery. Chromatin-modifying enzymes are dependent on metabolic intermediates for chromatin remodeling, linking nutrient availability and cellular metabolism to the cellular epigenetic landscape. Here we identify methionine as a key nutrient affecting T cell epigenetic reprogramming in CD4+ T helper (Th) cells. Using metabolomic approaches, we showed that methionine is rapidly taken up by activated T cells and then serves as the major substrate for the biosynthesis of S-adenosyl-L-methionine (SAM), the universal methyl donor for cellular methyltransferases. Conversely, methionine restriction (MR) depletes intracellular SAM pools, reduces global histone H3K4 methylation (H3K4me3) in T cells, and reduces H3K4me3 levels at the promoter regions of key genes involved in CD4+ Th17 cell proliferation and cytokine production. Applied to the mouse model of multiple sclerosis (experimental autoimmune encephalomyelitis), dietary methionine restriction reduced the expansion of pathogenic Th17 cells in vivo, leading to reduced T cell-mediated neuroinflammation and disease onset. Overall our data identify methionine as a key nutritional factor that shapes T cell proliferation, differentiation, and function in part through regulation of histone methylation in T cells.

2020-02-03 | GSE143321 | GEO

Methionine metabolism shapes T helper cell responses through regulation of epigenetic reprogramming [RNA-Seq]

2020-02-03 | GSE143320 | GEO

Methionine metabolism shapes T helper cell responses through regulation of epigenetic reprogramming [ChIP-Seq]

Project description:Methionine metabolism shapes T helper cell responses through regulation of epigenetic reprogramming [ChIP-Seq]

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Methionine metabolism shapes T helper cell responses through regulation of epigenetic reprogramming [RNA-Seq]

Project description:Methionine metabolism shapes T helper cell responses through regulation of epigenetic reprogramming [RNA-Seq]

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Methionine metabolism shapes T helper cell responses through regulation of epigenetic reprogramming

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-02-03 | GSE143322 | GEO

Transcriptional reprogramming of methionine restricted cells

Project description:The genome-wide transcriptional response of S. cerevisiae cells upon transfer to methionine-restricted media is investigated. DHO strain (BY4742 background) was cultivated batch-wise in SDC media at 30C and 180 rpm up to mid-exponential phase (OD600 ~ 0.6). The cells of the main culture were divided in three aliquots at the mid-exponential phase, centrifuged at 6000 rpm for 5 min, washed twice with deionized and distilled sterile water prior to their transfer to the treatment media. Treatment media comprised of SDC + 0.75% methionine for the methionine-restricted case while SDC is used for the control case. Sample collection for transcriptional profiling was done at the 2nd hour of the transfer. The experiments were carried out in biological triplicates.

2024-01-01 | E-MTAB-12860 | biostudies-arrayexpress

Methionine starvation caused reprogrammed metabolism in Streptococcus pneumoniae

Project description:In our study, deletion of methionine synthesis gene metE (SPD_0510) impaired the growth of Streptococcus pneumoniae strain D39 significantly when bacteria were cultured in chemically defined medium with a low concentration of methionine. Bacteria undergo methionine starvation in this condition. We aimed to know how S. pneumoniae responses to methionine starvation, particularly at the transcriptional level. RNA-seq results show that 804 genes (41.2 % of whole genome) were differentially expressed under methionine starvation. Among them, 258 genes (32.1 %) are related to cell metabolism, with 75 genes involved in sugar and carbon metabolism, 88 genes for synthesis of metabolic products and 95 genes for uptake of amino acids and sugars. Combined with other experiments data, this showed the reprogrammed metabolism in S. pneumoniae under methionine starvation.

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Epigenetic reprogramming shapes the cellular landscape of schwannoma

Project description:Cell state evolution underlies tumor development and response to therapy1, but mechanisms specifying cancer cell states and intratumor heterogeneity are incompletely understood. Schwannomas are the most common tumors of the peripheral nervous system and are treated with surgery and ionizing radiation2–5. Schwannomas can oscillate in size for many years after radiotherapy6,7, suggesting treatment may reprogram schwannoma cells or the tumor microenvironment. Here we show epigenetic reprogramming shapes the cellular landscape of schwannomas. We find schwannomas are comprised of 2 molecular groups distinguished by reactivation of neural crest development pathways or misactivation of nerve injury mechanisms that specify cancer cell states and the architecture of the tumor immune microenvironment. Schwannoma molecular groups can arise independently, but ionizing radiation is sufficient for epigenetic reprogramming of neural crest to immune-enriched schwannoma by remodeling chromatin accessibility, gene expression, and metabolism to drive schwannoma cell state evolution and immune cell infiltration. To define functional genomic mechanisms underlying epigenetic reprograming of schwannomas, we develop a technique for simultaneous interrogation of chromatin accessibility and gene expression coupled with genetic and therapeutic perturbations in single-nuclei. Our results elucidate a framework for understanding epigenetic drivers of cancer evolution and establish a paradigm of epigenetic reprograming of cancer in response to radiotherapy.

2023-04-18 | PXD014798 | Pride

SIRT1 regulates methionine metabolism and pluripotency of mouse embrynoic stem cells (mESCs)

Project description:The goal of this project is to understand the role of SIRT1, the most conserved mammalian NAD+-dependent protein deacetylase, in methionine metabolism and pluripotency of mESCs. Our recent studies indicate that SIRT1 deficient mESCs are hypersensitive to methionine restriction-induced differentiation and apoptosis, primarily due to a reduced conversion of methionine to S-adenosylmethionine. This reduction leads to marked decrease in methylation levels of histones in SIRT1 deficient mESCs. To understand the impact of histone methylation alterations on stem cell functions in SIRT1 KO mESCs, we examined the transcriptomes of SIRT1 WT and KO mESCs cultured in either complete M10 medium (com) or methionine restricted medium containing 6 uM methionine (6met) for 6, 24, and 72 hours by microarray analysis.

2017-10-10 | GSE77757 | GEO

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