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Alcohol metabolism directly fuels histone acetylation in the brain [RNA-Seq II]

ABSTRACT: Alcohol metabolism directly fuels histone acetylation in the brain [RNA-Seq II]

PROVIDER: PRJNA504860 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8180270.fastq.gz	Fastqsanger.gz
	SRR8180280.fastq.gz	Fastqsanger.gz
	SRR8180271.fastq.gz	Fastqsanger.gz
	SRR8180281.fastq.gz	Fastqsanger.gz
	SRR8180272.fastq.gz	Fastqsanger.gz

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Alcohol metabolism directly fuels histone acetylation in the brain

Project description:Alcohol metabolism directly fuels histone acetylation in the brain

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Alcohol metabolism directly fuels histone acetylation in the brain [RNA-Seq II]

Project description:In the adult brain, epigenetic control of gene expression has important roles in the processing of neural activity. Emerging evidence suggests that epigenetic regulation is dependent on metabolic state, implicating specific metabolic factors in neural functions that drive behavior. In neurons, histone acetylation is dependent on the metabolite acetyl-CoA that is produced from acetate by chromatin-bound ACSS21. Here, using in vivo stable isotope labeling in mouse, we show that alcohol metabolism rapidly fuels histone acetylation in the brain by direct deposition of alcohol-derived acetyl groups onto histones in an ACSS2-dependent manner. A similar induction was observed with heavy labeled acetate injection in vivo. Injection of labeled alcohol into a pregnant mouse results in incorporation of labeled acetyl groups into gestating fetal brains, indicating that the acetate passes through the placenta. In isolated primary hippocampal neurons ex vivo, extracellular acetate induced learning and memory-related transcriptional programs that were sensitive to ACSS2 inhibition. Strikingly, alcohol-related associative learning requires ACSS2 in vivo. These findings establish a novel and direct link between alcohol metabolism and neuronal ACSS2-dependent histone acetylation in the brain, providing evidence that dynamic acetate release from liver metabolism may travel to the brain for direct epigenetic regulation in neurons.

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Alcohol metabolism directly fuels histone acetylation in the brain [RNA-Seq]

Project description:Alcohol metabolism directly fuels histone acetylation in the brain [RNA-Seq]

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Alcohol metabolism directly fuels histone acetylation in the brain [ChIP-Seq]

Project description:Alcohol metabolism directly fuels histone acetylation in the brain [ChIP-Seq]

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Alcohol metabolism directly fuels histone acetylation in the brain [ChIP-Seq]

2019-08-01 | GSE122186 | GEO

Alcohol metabolism directly fuels histone acetylation in the brain [RNA-Seq]

2019-08-01 | GSE122181 | GEO

Alcohol metabolism directly fuels histone acetylation in the brain

Project description:This SuperSeries is composed of the SubSeries listed below. Reviewers: for a UCSC Genome Browser session of the chIP-seq and the ex vivo RNA-seq, please see: https://genome.ucsc.edu/cgi-bin/hgTracks?hgS_doOtherUser=submit&hgS_otherUserName=Gdonahue&hgS_otherUserSessionName=Alcohol%20Metabolism%20Publication

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Alcohol-sourced acetate impairs T cell function by promoting cortactin acetylation

Project description:Alcohol is among the most widely consumed dietary substances. While excessive alcohol consumption damages the liver, heart and brain, clinical observations also suggest that alcohol has strong immunoregulatory properties. However, little is known about the mechanistic effects of alcohol on the immune system. T cell functions such as migration, immune synapse formation and activation depend on the reorganization of the cytoskeleton. In this study, we show that acetate, the metabolite of alcohol, effectively inhibits the migratory capacity of T cells through increased tissue acetate levels that lead to acetylation of cortactin, a protein that binds filamentous actin and facilitates branching. Current knowledge of cortactin’s role in T cells is limited. Here we demonstrate and confirm that primary mouse and human T cells express cortactin and acetylation of cortactin inhibits actin filament binding leading to reduced filament branching, lamellipodia formation and T cell migration. Mutated acetylation-resistant cortactin rescued the acetate-induced inhibition of T cell migration. Primary mouse cortactin knock-out T cells exhibited severely reduced T cell migration. Furthermore, acetate-induced cytoskeletal changes effectively inhibited activation, proliferation, and immune synapse formation in T cells exposed to acetate at tissue concentrations reached by alcohol consumption. In summary, these data show that acetate, the key metabolite of alcohol, is inhibiting T cell mediated immune responses by modulating the biomechanics of T cells through their cytoskeletal function.

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Chronic alcohol metabolism results in DNA repair infidelity and cell-cycle-induced senescence in neurons

Project description:Chronic and excessive binge-like drinking is a risk factor to pathological cognitive decline and dementia, but the mechanism underlying the prolonged and lasting effect of alcohol even in abstainers remains elusive. This study investigates how ethyl alcohol directly results in metabolic reprograming and persistent physiological changes in brain cells that underlies such effect.

2023-02-22 | GSE202183 | GEO

Pantothenate metabolism fuels T cell antitumor immunity

Project description:Pantothenate metabolism fuels T cell antitumor immunity

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