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Mitochondrial complex III is essential for regulatory T cell suppressive function. [DNA methylation/RRBS]

ABSTRACT: Mitochondrial complex III is essential for regulatory T cell suppressive function. [DNA methylation/RRBS]

PROVIDER: PRJNA493088 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7903550.fastq.gz	Fastqsanger.gz
	SRR7903560.fastq.gz	Fastqsanger.gz
	SRR7903551.fastq.gz	Fastqsanger.gz
	SRR7903561.fastq.gz	Fastqsanger.gz
	SRR7903552.fastq.gz	Fastqsanger.gz

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Mitochondrial complex III is essential for regulatory T cell suppressive function. [DNA methylation/RRBS]

Project description:Regulatory T cells (Treg cells), a distinct subset of CD4+ T cells, are necessary for the maintenance of immune self-tolerance and homeostasis. Recent studies have demonstrated that Treg cells display a unique metabolic profile characterized by an increase in mitochondrial metabolism relative to other CD4+ effector subsets. Furthermore, the Treg cell lineage-defining transcription factor, Foxp3, has been shown to promote respiration; however, it remains unknown whether the mitochondrial respiratory chain is required for Treg cell suppressive capacity, stability, and survival. Here we report that Treg cell-specific ablation of mitochondrial respiratory chain complex III results in the development of a fatal inflammatory disease early in life, without impacting Treg cell number. Mice lacking complex III specifically in Treg cells displayed a loss of Treg cell suppressive capacity without altering Treg cell proliferation and survival. Treg cells deficient in complex III display decreased expression of genes associated with Treg function while maintaining stable FOXP3 expression. Complex III-null Treg cells displayed increased DNA methylation at the loci of differentially down-regulated genes without a global increase in DNA methylation. Loss of complex III in Treg cells resulted in buildup of the metabolites 2-hydroxyglutarate (2-HG) and succinate that can function as inhibitors of α-ketoglutarate (α−KG)-dependent dioxygenase reactions such as the ten-eleven translocation (TET) family of DNA demethylases. Thus, Treg cells require mitochondrial respiration to maintain immune regulatory gene expression and suppressive function.

2018-12-18 | GSE120451 | GEO

Mitochondrial complex III is essential for regulatory T cell suppressive function

Project description:Mitochondrial complex III is essential for regulatory T cell suppressive function

| PRJNA493083 | ENA

Mitochondrial complex III is essential for regulatory T cell suppressive function. [gene expression/RNA-seq]

2018-12-18 | GSE120449 | GEO

Mitochondrial complex III is essential for regulatory T cell suppressive function. [gene expression/RNA-seq]

Project description:Mitochondrial complex III is essential for regulatory T cell suppressive function. [gene expression/RNA-seq]

| PRJNA493086 | ENA

Mitochondrial complex III is essential for suppressive function of regulatory T cells.

Project description:Regulatory T cells (Treg cells), a distinct subset of CD4+ T cells, are necessary for the maintenance of immune self-tolerance and homeostasis1,2. Recent studies have demonstrated that Treg cells exhibit a unique metabolic profile, characterized by an increase in mitochondrial metabolism relative to other CD4+ effector subsets3,4. Furthermore, the Treg cell lineage-defining transcription factor, Foxp3, has been shown to promote respiration5,6; however, it remains unknown whether the mitochondrial respiratory chain is required for the T cell-suppression capacity, stability and survival of Treg cells. Here we report that Treg cell-specific ablation of mitochondrial respiratory chain complex III in mice results in the development of fatal inflammatory disease early in life, without affecting Treg cell number. Mice that lack mitochondrial complex III specifically in Treg cells displayed a loss of T cell-suppression capacity without altering Treg cell proliferation and survival. Treg cells deficient in complex III showed decreased expression of genes associated with Treg function, whereas Foxp3 expression remained stable. Loss of complex III in Treg cells increased DNA methylation as well as the metabolites 2-hydroxyglutarate (2-HG) and succinate that inhibit the ten-eleven translocation (TET) family of DNA demethylases7. Thus, Treg cells require mitochondrial complex III to maintain immune regulatory gene expression and suppressive function.

| S-EPMC6345596 | biostudies-literature

Mitochondrial complex III is essential for regulatory T cell suppressive function

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

2018-12-18 | GSE120452 | GEO

Maintenance DNA methylation is essential for regulatory T cell development and stability of suppressive function [DNA methylation/RRBS]

Project description:Maintenance DNA methylation is essential for regulatory T cell development and stability of suppressive function [DNA methylation/RRBS]

| PRJNA602402 | ENA

BRAWNIN: A sORF-encoded Peptide Essential for Vertebrate Mitochondrial Complex III

Project description:The emergence of small open reading frame (sORF)-encoded peptides (SEPs) is rapidly expanding the known proteome at the lower end of the size distribution. Here, we show that the mitochondrial proteome is enriched for proteins smaller than 100 a.a. (defined as SEPs). Using a prediction and validation pipeline for small open-reading-frame (sORF)-encoded peptides (SEPs), we report the discovery of 16 endogenous nuclear encoded, mitochondrial-localized SEPs (mito-SEPs). Through functional prediction, proteomics, metabolomics and metabolic flux modeling, we demonstrate that BRAWNIN (BR), a 71 amino acid peptide encoded by the C12orf73 gene, is essential for respiratory chain complex III (CIII) assembly. In human cells, BR is induced by the energy-sensing AMPK pathway, and its depletion impairs mitochondrial ATP production. In vivo, BR is enriched in muscle tissues and its maternal zygotic deletion in zebrafish causes complete CIII loss, resulting in severe growth retardation, lactic acidosis and early death. Our findings demonstrate that BR is essential for oxidative phosphorylation across vertebrate species. We propose that mito-SEPs are an untapped resource for essential regulators of oxidative metabolism. The dataset included in this entry is for the Zebrafish and MEF BR knockouts.

2020-03-18 | PXD016718 | Pride

The essential clathrin adaptor protein complex-2 is tumor suppressive specifically in vivo

Project description:The microenvironment is a rich source of new cancer targets. While whole-genome CRISPR/Cas9 screens have identified vulnerabilities in cultured cells, it is a challenge to use this approach in tumors to interrogate the microenvironment. To this end, we screened a panel of pancreatic cancer lines grown in culture versus as tumors with a phosphatidylinositol metabolism CRISPR/Cas9 library. This revealed the Adaptor Protein complex-2 (AP2) of clathrin-mediated endocytosis behaves as common essential in culture but tumor suppressive in vivo. These polar-opposite phenotypes were attributed to different microenvironments. In culture, AP2 loss reduces endocytosis of transferrin and iron import. In tumors, alternative iron transport pathways allow pro-tumor signaling to manifest. In the most sensitive case, AP2 loss reprograms the plasma membrane proteome, retaining integrins on the surface leading to downregulation of the tumor-suppressor PTEN. Analysis of human tumors suggests a similar tumor suppressive activity. AP2 may foreshadow other proteins unique to the tumor-microenvironment.

2024-12-12 | GSE233173 | GEO

The essential clathrin adaptor protein complex-2 is tumor suppressive specifically in vivo

Project description:The essential clathrin adaptor protein complex-2 is tumor suppressive specifically in vivo

| PRJNA975168 | ENA