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Tet2 regulates Sin3a recruitment at active enhancers in embryonic stem cells

ABSTRACT: Tet2 regulates Sin3a recruitment at active enhancers in embryonic stem cells

PROVIDER: PRJNA880822 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21586205_1.fastq.gz	Fastqsanger.gz
	SRR21586205_2.fastq.gz	Fastqsanger.gz
	SRR21586206_1.fastq.gz	Fastqsanger.gz
	SRR21586206_2.fastq.gz	Fastqsanger.gz
	SRR21586207_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Tet2 regulates Sin3a recruitment at active enhancers in embryonic stem cells

Project description:In this study: (1) we distinguished Tet2 target genes that are regulated by its catalytic vs. noncatalytic functions in ESCs by transcriptomic profiling of Tet2 wildtype (WT), Tet2 catalytic mutant (Mut), and Tet2 knockout (KO) mouse ESCs by RNA-seq. (2) We mapped genome-wide DNA methylation of Tet2-WT, Tet2-Mut, and Tet2-KO ESCs by WGBS, to establish a critical role for Tet2 in demethylating promoters and enhancers of its catalytic target genes. (3) We determined how the genome-wide occupancy of the epigenetic modifiers Sin3a and Sap30 and the enrichment of H3K27ac, are affected in Tet2-Mut and Tet2-KO ESCs versus Tet2-WT by CUT&Tag and identified that Tet2 deficiency diminishes Sin3a occupancy at promoters and enhancers. (4) We mapped Sin3a levels genome-wide in Tet1/2 double catalytic mutant (DMUT) and Tet1/2 double knockout (DKO) ESCs, and found that deficiency of both Tet1 and Tet2 resulted in decreased levels of Sin3a in a subset of active enhancers.

2023-06-23 | GSE213398 | GEO

TET2 coactivates gene expression through demethylation of enhancers

Project description:The tet methylcytosine dioxygenase 2 (TET2) enzyme catalyzes the conversion of the modified DNA base 5-methylcytosine to 5-hydroxymethylcytosine. TET2 is frequently mutated or dysregulated in multiple human cancers, and loss of TET2 is associated with changes in DNA methylation patterns. Here, using newly developed TET2-specific antibodies and the estrogen response as a model system for studying the regulation of gene expression, we demonstrate that endogenous TET2 occupies active enhancers and facilitates the proper recruitment of ERalpha. Knockout of TET2 by CRISPR-CAS9 leads to a global increase of DNA-methylation at enhancers resulting in attenuation of the estrogen response. We further identified a positive feedback loop between TET2 and ERalpha, which further requires MLL3/COMPASS at these enhancers. Together, this study reveals an epigenetic axis coordinating a transcriptional program through enhancer activation via DNA demethylation.

2018-10-04 | GSE120756 | GEO

Loss of TET2 in hematopoietic cells leads to DNA hypermethylation of active enhancers and induction of leukemogenesis (Affymetrix)

Project description:DNA methylation is tightly regulated throughout mammalian development and altered methylation patterns are a hallmark of cancer. The methylcytosine dioxygenase TET2 is frequently mutated in acute myeloid leukemia (AML) and has been suggested to protect CpG islands and promoters from aberrant methylation. By generating a novel mouse model of Tet2-deficient AML we show that loss of Tet2 in hematopoietic cells leads to progressive hypermethylation of active enhancer elements and altered expression of genes implicated in tumorigenesis. In contrast, CpG island and promoter methylation does not change in a Tet2-dependent manner. Furthermore, we confirm this specific enhancer hypermethylation phenotype in human AML patients. Thus, we propose that TET2 prevents leukemic transformation of hematopoietic cells by protecting enhancers from aberrant DNA methylation. Gene expression profiles from Tet2-/-;AML1-ETO and Tet2fl/fl;AML1-ETO in vitro-grown hematopoietic cells were compared using GeneChip Mouse Gene ST 2.0 Arrays (Affymetrix). Expression changes were investigated at early (passage 2) and late (passage 10) timepoints after Tet2 disruption.

2015-04-22 | E-GEOD-59586 | biostudies-arrayexpress

TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells

Project description:TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells

| PRJNA476603 | ENA

Loss of TET2 in hematopoietic cells leads to DNA hypermethylation of active enhancers and induction of leukemogenesis (eRRBS)

Project description:DNA methylation is tightly regulated throughout mammalian development and altered methylation patterns are a hallmark of cancer. The methylcytosine dioxygenase TET2 is frequently mutated in acute myeloid leukemia (AML) and has been suggested to protect CpG islands and promoters from aberrant methylation. By generating a novel mouse model of Tet2-deficient AML we show that loss of Tet2 in hematopoietic cells leads to progressive hypermethylation of active enhancer elements and altered expression of genes implicated in tumorigenesis. In contrast, CpG island and promoter methylation does not change in a Tet2-dependent manner. Furthermore, we confirm this specific enhancer hypermethylation phenotype in human AML patients. Thus, we propose that TET2 prevents leukemic transformation of hematopoietic cells by protecting enhancers from aberrant DNA methylation. Enhanced Reduced Representation Bisulfite Sequencing (eRRBS) analysis of in vitro-grown hematopoietic cells transduced with AML1-ETO or MLL-AF9

2015-04-22 | E-GEOD-59584 | biostudies-arrayexpress

Loss of TET2 in hematopoietic cells leads to DNA hypermethylation of active enhancers and induction of leukemogenesis (MeDIP-seq)

Project description:DNA methylation is tightly regulated throughout mammalian development and altered methylation patterns are a hallmark of cancer. The methylcytosine dioxygenase TET2 is frequently mutated in acute myeloid leukemia (AML) and has been suggested to protect CpG islands and promoters from aberrant methylation. By generating a novel mouse model of Tet2-deficient AML we show that loss of Tet2 in hematopoietic cells leads to progressive hypermethylation of active enhancer elements and altered expression of genes implicated in tumorigenesis. In contrast, CpG island and promoter methylation does not change in a Tet2-dependent manner. Furthermore, we confirm this specific enhancer hypermethylation phenotype in human AML patients. Thus, we propose that TET2 prevents leukemic transformation of hematopoietic cells by protecting enhancers from aberrant DNA methylation. 5hmC-DIP-seq analysis for distribution of 5hmC in in vitro-grown hematopoietic cells transduced with AML1-ETO

2015-04-22 | E-GEOD-59579 | biostudies-arrayexpress

Loss of TET2 in hematopoietic cells leads to DNA hypermethylation of active enhancers and induction of leukemogenesis (ChIP-seq)

Project description:DNA methylation is tightly regulated throughout mammalian development and altered methylation patterns are a hallmark of cancer. The methylcytosine dioxygenase TET2 is frequently mutated in acute myeloid leukemia (AML) and has been suggested to protect CpG islands and promoters from aberrant methylation. By generating a novel mouse model of Tet2-deficient AML we show that loss of Tet2 in hematopoietic cells leads to progressive hypermethylation of active enhancer elements and altered expression of genes implicated in tumorigenesis. In contrast, CpG island and promoter methylation does not change in a Tet2-dependent manner. Furthermore, we confirm this specific enhancer hypermethylation phenotype in human AML patients. Thus, we propose that TET2 prevents leukemic transformation of hematopoietic cells by protecting enhancers from aberrant DNA methylation. ChIP-seq analysis for distribution of H3K4me1, H3K27ac, and H3K4me3 histone marks in in vitro-grown hematopoietic cells transduced with AML1-ETO

2015-04-22 | E-GEOD-59580 | biostudies-arrayexpress

TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells [TET2 ChIP-seq ES cells]

Project description:TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells [TET2 ChIP-seq ES cells]

| PRJNA476604 | ENA

TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells [TET2 ChIP-seq hematopoietic cells]

Project description:TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells [TET2 ChIP-seq hematopoietic cells]

| PRJNA476607 | ENA

Loss of TET2 in hematopoietic cells leads to DNA hypermethylation of active enhancers and induction of leukemogenesis [Agilent]

Project description:DNA methylation is tightly regulated throughout mammalian development and altered DNA methylation patterns are a general hallmark of cancer. The methylcytosine dioxygenase TET2 is frequently mutated in hematological disorders, including acute myeloid leukemia (AML), and has been suggested to protect CpG islands and promoters from aberrant DNA methylation. In this study, we present a novel Tet2-dependent leukemia mouse model that closely recapitulates gene expression profiles and hallmarks of human AML1-ETO induced AML. Using this model, we show that the primary effect of Tet2 loss in pre-leukemic hematopoietic cells is progressive and widespread DNA hypermethylation affecting up to 25% of active enhancer elements. In contrast, CpG island and promoter methylation does not change in a Tet2-dependent manner, but increase relative to population doublings. We confirm this specific enhancer hypermethylation phenotype in human AML patients with TET2 mutations. Analysis of immediate gene expression changes reveals rapid deregulation of a large number of genes implicated in tumorigenesis, including many downregulated tumor suppressor genes. Hence, we propose that TET2 prevents leukemic transformation by protecting enhancers from aberrant DNA methylation, and that it is the combined silencing of several tumor suppressor genes in TET2-mutated hematopoietic cells that contribute to increased stem cell proliferation and leukemogenesis. Gene expression profiles (Agilent SurePrint G3 Mouse GE 8x60K arrays) of FACS-sorted in vivo GMP cells (Lin-cKit+Sca1-CD16/32+CD150-) isolated from bone marrow of recipient mice one month after transplantation of WT bone marrow or splenic cells from two independent moribond Tet2-/-:AE leukemic mice (LeuA/AE1), or LeuB/AE3)

2015-04-30 | E-GEOD-68415 | biostudies-arrayexpress

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