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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE143322 | GEO | 2020/02/03

REPOSITORIES: GEO

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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

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

| PRJNA600853 | ENA

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 [ChIP-Seq]

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

| PRJNA600857 | ENA

The glucose transporter GLUT3 controls T helper 17 cell responses through glycolytic-epigenetic reprogramming.

Project description:Metabolic reprogramming is a hallmark of activated T cells. The switch from oxidative phosphorylation to aerobic glycolysis provides energy and intermediary metabolites for the biosynthesis of macromolecules to support clonal expansion and effector function. Here, we show that glycolytic reprogramming additionally controls inflammatory gene expression via epigenetic remodeling. We found that the glucose transporter GLUT3 is essential for the effector functions of Th17 cells in models of autoimmune colitis and encephalomyelitis. At the molecular level, we show that GLUT3-dependent glucose uptake controls a metabolic-transcriptional circuit that regulates the pathogenicity of Th17 cells. Metabolomic, epigenetic, and transcriptomic analyses linked GLUT3 to mitochondrial glucose oxidation and ACLY-dependent acetyl-CoA generation as a rate-limiting step in the epigenetic regulation of inflammatory gene expression. Our findings are also important from a translational perspective because inhibiting GLUT3-dependent acetyl-CoA generation is a promising metabolic checkpoint to mitigate Th17-cell-mediated inflammatory diseases.

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Epigenetic reprogramming shapes the cellular landscape of schwannoma.

Project description:Mechanisms specifying cancer cell states and response to therapy are incompletely understood. Here we show epigenetic reprogramming shapes the cellular landscape of schwannomas, the most common tumors of the peripheral nervous system. We find schwannomas are comprised of 2 molecular groups that are distinguished by activation of neural crest or nerve injury pathways that specify tumor cell states and the architecture of the tumor immune microenvironment. Moreover, we find radiotherapy is sufficient for interconversion of neural crest schwannomas to immune-enriched schwannomas through epigenetic and metabolic reprogramming. To define mechanisms underlying schwannoma groups, 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 tumor evolution and establish a paradigm of epigenetic and metabolic reprograming of cancer cells that shapes the immune microenvironment in response to radiotherapy.

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HOXB13 inhibits lipid metabolism through HDAC3-mediated epigenetic reprogramming

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

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Metabolic Reprogramming Drives Pituitary Tumor Growth through Epigenetic Regulation of TERT.

Project description:Pituitary adenomas are common, benign brain tumors. Some tumors show aggressive phenotypes including early recurrence, local invasion and distant metastasis, but the underlying mechanism to drive the progression of pituitary tumors has remained to be clarified. Aerobic glycolysis known as the Warburg effect is one of the emerging hallmarks of cancer, which has an impact on the tumor biology partly through epigenetic regulation of the tumor-promoting genes. Here, we demonstrate metabolic reprogramming in pituitary tumors contributes to tumor cell growth with epigenetic changes such as histone acetylation. Notably, a shift in histone acetylation increases the expression of telomerase reverse transcriptase (TERT) oncogene, which drives metabolism-dependent cell proliferation in pituitary tumors. These indicate that epigenetic changes could be the specific biomarker for predicting the behavior of pituitary tumors and exploitable as a novel target for the aggressive types of the pituitary tumors.

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Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-02-13 | E-GEOD-52304 | biostudies-arrayexpress