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

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

PROVIDER: PRJNA602402 | ENA |

REPOSITORIES: ENA

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

Project description:Regulatory T (Treg) cells require Foxp3 expression and induction of a specific DNA hypomethylation signature during development, after which Treg cells persist as a self-renewing population that regulates immune system activation. Whether maintenance DNA methylation is required for Treg cell lineage development and stability and how methylation patterns are maintained during lineage self-renewal remain unclear. Here, we demonstrate that the epigenetic regulator Uhrf1 is essential for maintenance of methyl-DNA marks that stabilize Treg cellular identity by repressing effector T cell transcriptional programs. Constitutive and induced deficiency of Uhrf1 within Foxp3+ cells resulted in global yet non-uniform loss of DNA methylation, derepression of inflammatory transcriptional programs, destabilization of the Treg cell lineage, and spontaneous inflammation. These findings support a paradigm in which maintenance DNA methylation is required in distinct regions of the Treg cell genome for both lineage establishment and stability of identity and suppressive function.

2020-08-27 | GSE143973 | GEO

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

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

| PRJNA493088 | ENA

Maintenance DNA methylation is essential for regulatory T cell development and stability of suppressive function [gene expression/RNA-seq]

2020-08-27 | GSE143972 | GEO

DNA methylation reprogramming after spinal nerve injury [RRBS]

Project description:DNA methylation reprogramming after spinal nerve injury [RRBS]

| PRJNA472956 | ENA

DNA methylation profile for male SD Rats upon fructose treatment by RRBS

Project description:DNA methylation profile for male SD Rats upon fructose treatment by RRBS

2016-10-19 | GSE59893 | GEO

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

DNA methylation profiling to investigate how Tet1 controls maintenance DNA methylation via the regulation of Dppa3 in ESCs

Project description:DNA methylation profiling using RRBS in wild type and Dppa3 knockout ESCs.

2020-09-30 | E-MTAB-6800 | biostudies-arrayexpress

Maintenance DNA methylation is essential for regulatory T cell development and stability of suppressive function

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

| PRJNA602400 | ENA

Tet1 controls maintenance DNA methylation via the regulation of Dppa3

Project description:Dissection of catalytic and non-catalytic functions of Tet1. DNA methylation (RRBS) profiling of wild type, Tet1 knockout and catalytic mutants during EpiLC differentiation.

2020-09-30 | E-MTAB-6785 | biostudies-arrayexpress

Extensive changes in DNA methylation are associated with expression of mutant huntingtin [RRBS]

Project description:The earliest stages of Huntington’s disease are marked by changes in gene expression that are caused in an indirect and poorly understood manner by polyglutamine expansions in the huntingtin protein (HTT). To explore the hypothesis DNA methylation may be altered in cells expressing mutated HTT, we use reduced-representation bisulfite sequencing (RRBS) to map sites of DNA methylation in cells carrying either wild-type or mutant HTT. We find that a large fraction of the genes that change in expression in the presence of mutant huntingtin demonstrate significant changes in DNA methylation. Regions with low CpG content, which have previously been shown to undergo methylation changes in response to neuronal activity, are disproportionately affected. Based on the sequence of regions that change in methylation, we identify AP-1 and SOX2 as transcriptional regulators associated with DNA methylation changes, and we confirm these hypotheses using genome-wide chromatin immunoprecipitation (ChIP-Seq). Our findings suggest new mechanisms for the effects of polyglutamine-expanded HTT. These results also raise important questions about the potential effects of changes in DNA methylation on neurogenesis and at later stages, cognitive decline in Huntington’s patients. RRBS in STHdhQ7/Q7 and STHdhQ111/Q111 cells

2013-01-24 | E-GEOD-43432 | biostudies-arrayexpress

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