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Mitochondrial ATP production promotes T cell differentiation and function by regulating chromatin accessibility [RNAseq2]

ABSTRACT: Mitochondrial ATP production promotes T cell differentiation and function by regulating chromatin accessibility [RNAseq2]

PROVIDER: PRJNA1299895 | ENA |

REPOSITORIES: ENA

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Mitochondrial ATP production promotes T cell differentiation and function by regulating chromatin accessibility [RNAseq2]

Project description:Immune elimination of chronic infection or cancer requires cytotoxic CD8 T cells that adopt and maintain an effector phenotype. Cytotoxic T cell function is a bioenergetically demanding process and T cells subjected to chronic antigen exposure have compromised effector function despite high rates of glycolysis. Here we report the ability of the short chain fatty acid, D-α-hydroxybutyrate, to act as a signaling molecule that increases mitochondrial ATP production and drives the conversion of proliferating T cells into cytotoxic effector cells. DAHB signaling switches ATP production from glycolysis to fatty acid oxidation, even in glucose-replete media. This conversion suppresses both AMPK phosphorylation and the integrated stress response (ISR) in activated T cells while significantly elevating the level of the phosphagen, phosphocreatine (PCr). Both the PCr bioenergetic reserve and oxidative phosphorylation were required for T cell effector differentiation. DAHB-induction of CD8-effector gene transcription was coupled to bioenergetics by enhanced ATP-dependent remodeling of chromatin accessibility at effector gene loci. DAHB enhanced CD8 T cell antitumor activity both in vitro and in vivo, and DAHB treatment of transferred T cells led to persistent in vivo antitumor effects. Together, these findings link cellular bioenergetics to the regulation of chromatin accessibility and gene expression required to support effector function.

2025-08-05 | GSE304271 | GEO

Mitochondrial ATP production promotes T cell differentiation and function by regulating chromatin accessibility [ATACseq2]

Project description:Mitochondrial ATP production promotes T cell differentiation and function by regulating chromatin accessibility [ATACseq2]

| PRJNA1299806 | ENA

Mitochondrial ATP production promotes T cell differentiation and function by regulating chromatin accessibility [ATACseq1]

Project description:Mitochondrial ATP production promotes T cell differentiation and function by regulating chromatin accessibility [ATACseq1]

| PRJNA1299807 | ENA

Mitochondrial ATP production promotes T cell differentiation and function by regulating chromatin accessibility [RNAseq1]

Project description:Mitochondrial ATP production promotes T cell differentiation and function by regulating chromatin accessibility [RNAseq1]

| PRJNA1299814 | ENA

Mitochondrial ATP production promotes T cell differentiation and function by regulating chromatin accessibility [RNAseq1]

2025-08-05 | GSE304270 | GEO

Mitochondrial ATP production promotes T cell differentiation and function by regulating chromatin accessibility [ATACseq2]

2025-08-05 | GSE304269 | GEO

Mitochondrial ATP production promotes T cell differentiation and function by regulating chromatin accessibility [ATACseq1]

2025-08-05 | GSE304268 | GEO

lyrum larum ypsium Carina RNAseq2

Project description:lyrum larum ypsium Carina RNAseq2

| PRJEB58060 | ENA

Piwi modulates chromatin accessibility by regulating multiple factors including histone H1 to repress transposons

Project description:PIWI-interacting RNAs (piRNAs) mediate transposable element (TE) silencing at the transcriptional or post-transcriptional level in animal gonads. In the Drosophila ovary, Piwiâ??piRNA complexes (Piwiâ??piRISCs) repress TE transcription by modifying the chromatin state, such as H3K9me3 marks. Here, we demonstrate that Piwi physically interacts with linker histone H1. Depletion of Piwi decreases H1 density on target loci, leading to TE derepression. Loss of H1 results in gain of chromatin accessibility at target loci without affecting H3K9me3 and heterochromatin protein 1a (HP1a) density at the same loci. Piwi-mediated TE silencing also requires HP1a by regulating chromatin accessibility through its association with target loci. Thus, Piwiâ??piRISCs require both H1 and HP1a to repress TEs, and the silencing is correlated with the state of chromatin formation rather than H3K9me3 marks. These findings suggest that Piwiâ??piRISCs regulate the interaction of chromatin components with target loci to maintain silencing of the TE state through the modulation of chromatin accessibility. RNA levels, H1 and H3K9me3 occupancy, chromatin accessibility, and Piwi-associated small RNA levels in ovarian somatic cells (OSC) depleted of piRNA pathway components and H1.

2016-06-30 | E-GEOD-81434 | biostudies-arrayexpress

The Role of LINC01235 in Regulating Chromatin Accessibility

Project description:The Role of LINC01235 in Regulating Chromatin Accessibility

| PRJNA1132191 | ENA