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Genome-wide analysis of methylated DNA in control and Tet2/Tet3-deficient B cells

ABSTRACT: Genome-wide analysis of methylated DNA in control and Tet2/Tet3-deficient B cells

PROVIDER: PRJNA566023 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10134791_1.fastq.gz	Fastqsanger.gz
	SRR10134791_2.fastq.gz	Fastqsanger.gz
	SRR10134792_1.fastq.gz	Fastqsanger.gz
	SRR10134792_2.fastq.gz	Fastqsanger.gz
	SRR10134793_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Genome-wide mapping of gene expression in control and Tet2/Tet3-deficient B cell subsets

Project description:We report the global gene expression in Tet2/Tet3-sufficient and -deficient B cell subsets. We found an alteration of multiple gene expressions in the absence of Tet2 and Tet3 in B cells. This study provides a basis for the comprehensive understanding of Tet function in B cells.

2020-07-08 | GSE137914 | GEO

Genome-wide analysis of methylated DNA in control and Tet2/Tet3-deficient B cells

Project description:We report the global DNA methylation status in B cells. We found that DNA demethylation occurred around gene promoters and Tet-dependent demethylation sites at the genome-wide manner. This study provides a basis for the comprehensive understanding of role of Tet2 and Tet3 in DNA demethylation-dependent regulation of transcription in B cells.

2020-07-08 | GSE137621 | GEO

TET2 and TET3 regulate GlcNAcylation and H3K4 methylation through OGT and SET1/COMPASS

Project description:TET proteins convert 5-methylcytosine to 5-hydroxymethylcytosine, an emerging dynamic epigenetic state of DNA that can influence transcription. Evidence has linked TET1 function to epigenetic repression complexes, yet mechanistic information, especially for the TET2 and TET3 proteins, remains limited. Here, we show a direct interaction of TET2 and TET3 with O-GlcNAc transferase (OGT). OGT does not appear to influence hmC activity, rather TET2 and TET3 promote OGT activity. TET2/3-OGT co-localize on chromatin at active promoters enriched for H3K4me3 and reduction of either TET2/3 or OGT activity results in a direct decrease in H3K4me3 and concomitant decreased transcription. Further, we show that Host Cell Factor 1 (HCF1), a component of the H3K4 methyltransferase SET1/COMPASS complex, is a specific GlcNAcylation target of TET2/3-OGT, and modification of HCF1 is important for the integrity of SET1/COMPASS. Additionally, we find both TET proteins and OGT activity promote binding of the SET1/COMPASS H3K4 methyltransferase, SETD1A, to chromatin. Finally, studies in Tet2 knockout mouse bone marrow tissue extend and support the data as decreases are observed of global GlcNAcylation and also of H3K4me3, notably at several key regulators of haematopoiesis. Together, our results unveil a step-wise model, involving TET-OGT interactions, promotion of GlcNAcylation, and influence on H3K4me3 via SET1/COMPASS, highlighting a novel means by which TETs may induce transcriptional activation. ChIP-Seq experiments were performed on Illumina HiScanSQ sequencer in wild-type HEK293T cells for H3K4me3 histone marks, O-GlcNAc and HCF1, for HT-TET2, HT-TET3 and HT-OGT in HEK293T cells overexpressing those three fusion proteins and in TET2 Kd HEK293T cells for H3K4me3 histone marks. ChIP-Seqs were also performed in mouse bone marrow tissues for H3K4me3 histone marks, O-GlcNAc, endogenous Tet2 and in Tet2 Ko bone marrow tissues for H3K4me3 histone marks.

2013-02-07 | E-GEOD-36620 | biostudies-arrayexpress

Genome-wide mapping of gene expression in control and Tet2/Tet3-deficient B cell subsets

Project description:Genome-wide mapping of gene expression in control and Tet2/Tet3-deficient B cell subsets

| PRJNA573854 | ENA

Genome-wide mapping of binding of HDAC1/HDAC2 and H3K9/14Ac modification in control and Tet2/Tet3-deficient B cells

Project description:We report the genome-wide accumulation of HDAC1, HDAC2 and H3K9/14Ac in B cells. We found that the binding of HDAC1 and HDAC2 was observed mainly on proximal promoters, suggesting a redundant role of these HDACs in transcriptional regulation. This study provides a basis for the comprehensive understanding of Tet2/Tet3-HDACs-mediated B cell regulation.

2020-07-08 | GSE137666 | GEO

Tet2 and Tet3 mediated active cytosine hydroxymethylation in Six2 progenitor cells is critical for nephron progenitor differentiation and nephron endowment

Project description:Nephron endowment is a key determinant of later life hypertension and kidney disease. Here we studied whether epigenetic changes, specifically the ten–eleven translocation (Tet) DNA demethylase family, Tet1, Tet2, and Tet3-mediated active DNA hydroxymethylation is necessary for gene expression regulation and kidney differentiation. We generated mice with deletion of Tet1, Tet2 or Tet3 in Six2 positive nephron progenitors (NP). We did not observe changes in development or kidney function in mice with nephron progenitor-specific deletion of Tet1, Tet2, Tet3 or Tet1/Tet2 or Tet1/Tet3. On the other hand, mice with combined Tet2 and Tet3 loss in Six2-positive NPCs failed to form nephrons leading to kidney failure and perinatal death. Tet2 and Tet3 loss in Six2-positive NPs resulted in defect in mesenchymal to epithelial transition and renal vesicle differentiation. Whole genome bisulfite sequencing, single cell RNA sequencing, and gene and protein expression assay identified a defect in expression in genes in the WNT-β-catenin signaling pathway in absence of Tet2 and Tet3 due to a failure in demethylation of these loci. Our results indicate the key role of Tet2 and Tet3-mediated active cytosine hydroxymethylation in NPs in kidney development and nephron endowment.

2022-11-23 | GSE212715 | GEO

TET2 and TET3 regulate GlcNAcylation and H3K4 methylation through OGT and SET1/COMPASS

2013-02-07 | GSE36620 | GEO

Concomitant loss of TET2 and TET3 results in T cell expansion and genomic instability

Project description:TET proteins are tumor suppressors that through their catalytic activity oxidize 5-methylcytosine to 5-hydroxymethylcytosine, to promote DNA demethylation and to regulate gene expression. Notably, TET2 is the second most frequently mutated gene in hematological malignancies, including T cell lymphomas. However, murine models with deletion of TET2 do not exhibit T cell expansion, presumably due to redundancy with other members of the TET family of proteins. In order to gain insight on the TET mediated molecular events that safeguard T cells from aberrant proliferation we performed serial adoptive transfers of murine CD4 T cells that lack concomitantly TET2 and TET3 to fully immunocompetent congenic mice. Our data reveal a progressive acquisition of malignant traits upon loss of TET2 and TET3 that is characterized by loss of genomic integrity, acquisition of aneuploidy and upregulation of the protooncogene Myc.

2024-11-11 | GSE278239 | GEO

RNA-seq expression profiling of Xenopus tropicalis blastula embryos upon Tet2 and Tet3 knockdown

Project description:To analyze the role of Tet proteins on global gene expression, we profiled the transcriptome of Xenopus tropicalis blastula embryos upon knockdown of Tet2 and Tet3 using Morpholino antisense oligonucleotides.

2024-08-29 | GSE226466 | GEO

Concomitant loss of TET2 and TET3 results in T cell expansion and genomic instability [WGS]

Project description:TET proteins are tumor suppressors that through their catalytic activity oxidize 5-methylcytosine to 5-hydroxymethylcytosine, to promote DNA demethylation and to regulate gene expression. Notably, TET2 is one of the most frequently mutated genes in hematological malignancies, including T cell lymphomas. However, murine models with deletion of TET2 do not exhibit T cell expansion, presumably due to redundancy with other members of the TET family of proteins. In order to gain insight on the TET mediated molecular events that safeguard T cells from aberrant proliferation we performed serial adoptive transfers of murine CD4 T cells that lack concomitantly TET2 and TET3 to fully immunocompetent congenic mice. Our data reveal a progressive acquisition of malignant traits upon loss of TET2 and TET3 that is characterized by loss of genomic integrity, acquisition of aneuploidy and upregulation of the protooncogene Myc.

2024-11-07 | GSE276581 | GEO

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