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TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells

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

PROVIDER: PRJNA476603 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7359510.fastq.gz	Fastqsanger.gz
	SRR7359520.fastq.gz	Fastqsanger.gz
	SRR7359530_1.fastq.gz	Fastqsanger.gz
	SRR7359530_2.fastq.gz	Fastqsanger.gz
	SRR7359540_1.fastq.gz	Fastqsanger.gz

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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]

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TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells [RNA-Seq]

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

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TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells [ATAC-Seq]

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

| PRJNA476605 | ENA

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:The epigenetic regulator TET2 is frequently mutated in hematological diseases. Mutations have been shown to arise in hematopoietic stem cells early in disease development, lead to altered DNA methylation landscapes and to an increased risk of hematopoietic malignancy. Here, we show by genome-wide mapping of TET2 binding sites in different cell types that TET2 localizes to regions of open chromatin and cell-type specific enhancers. We find that deletion of Tet2 in native hematopoiesis as well as fully transformed Acute Myeloid Leukemia (AML) results in changes in transcription factor (TF) activity within these regions, and we provide evidence that loss of TET2 leads to attenuation of chromatin binding of members of the basic helix-loop-helix (bHLH) TF family. Together, these findings demonstrate that TET2 activity shapes the local chromatin environment at enhancers to facilitate TF binding and provide a compelling example of how epigenetic dysregulation can affect gene expression patterns and drive disease development.

2019-01-22 | GSE115965 | GEO

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

2019-01-22 | GSE115964 | GEO

TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells [ATAC-Seq]

2019-01-22 | GSE115962 | GEO

TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells [RNA-Seq]

2019-01-22 | GSE115967 | GEO

TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells.

Project description:The epigenetic regulator TET2 is frequently mutated in hematological diseases. Mutations have been shown to arise in hematopoietic stem cells early in disease development and lead to altered DNA methylation landscapes and an increased risk of hematopoietic malignancy. Here, we show by genome-wide mapping of TET2 binding sites in different cell types that TET2 localizes to regions of open chromatin and cell-type-specific enhancers. We find that deletion of Tet2 in native hematopoiesis as well as fully transformed acute myeloid leukemia (AML) results in changes in transcription factor (TF) activity within these regions, and we provide evidence that loss of TET2 leads to attenuation of chromatin binding of members of the basic helix-loop-helix (bHLH) TF family. Together, these findings demonstrate that TET2 activity shapes the local chromatin environment at enhancers to facilitate TF binding and provides an example of how epigenetic dysregulation can affect gene expression patterns and drive disease development.

| S-EPMC6442383 | biostudies-literature

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

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