Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA401733 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6004460_1.fastq.gz | Fastqsanger.gz | |||
| SRR6004460_2.fastq.gz | Fastqsanger.gz | |||
| SRR6004470_1.fastq.gz | Fastqsanger.gz | |||
| SRR6004470_2.fastq.gz | Fastqsanger.gz | |||
| SRR6004480_1.fastq.gz | Fastqsanger.gz |
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Project description:Background: Aberrant DNA methylation is an epigenetic hallmark of most malignant tumors including breast cancer. However, the exact role of TET2-mediated DNA demethylation in ERα-positive luminal breast cancer is not well understood. Results: Here we showed by TCGA analyses that lower TET2 mRNA expression level is associated with worse clinical outcomes (i.e., overall survival) in ERα-positive but not ERα-negative breast cancer. Moreover, depletion of TET2 by CRISPR/Cas9 results in increased tumorigenesis capability of MCF7 cells in vitro. Whole genome bisulfite sequencing (WGBS) analysis revealed that DNA hypermethylation (gain-of-5mC) occurs within a subgroup of enhancers including estrogen responsive element (EREs) in MCF7 cells upon TET2 depletion. ChIP-seq and RNA-seq analysis showed that TET2 depletion impairs E2-induced ERα binding to these ‘gain-of-5mC’ EREs and gene transcription. Conclusions: Our data suggest that TET2-mediated enhancer DNA demethylation fine-tunes ERα-dependent and independent gene transcription in ERα-positive breast cancer cells.
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Project description:In mammals, cytosine methylation (5mC) is widely distributed throughout the genome but is notably depleted from active promoters and enhancers. While the role of DNA methylation in promoter silencing has been well documented, the function of this epigenetic mark at enhancers remains unclear. Recent experiments have demonstrated that enhancers are enriched for 5-hydroxymethylcytosine (5hmC), an oxidization product of the Tet family of 5mC dioxygenases and an intermediate of DNA demethylation. These results support the involvement of Tet proteins in the regulation of dynamic DNA methylation at enhancers. By mapping DNA methylation and hydroxymethylation at base resolution, we find that deletion of Tet2 causes extensive loss of 5hmC at enhancers, accompanied by enhancer hypermethylation, reduction of enhancer activity, and delayed gene induction in the early steps of differentiation. Our results reveal that DNA demethylation modulates enhancer activity, and its disruption influences the timing of transcriptome reprogramming during cellular differentiation. We performed traditional bisulfite sequencing, TAB-Seq, RNA-Seq, and ChIP-Seq for 6 histone modifications in two biological replicates of wild-type, Tet1-/-, and Tet2-/- mouse ES cells. We also performed RNA-Seq analysis during a timecourse of differentiation to neural progenitor cells.
2014-09-25 | E-GEOD-48519 | biostudies-arrayexpress
Project description:T cell function is regulated by epigenetic mechanisms. 5-methylcytosine (5mC) conversion to 5-hydroxymethylcytosine (5hmC) by ten-eleven translocation (Tet) proteins was identified to mediate DNA demethylation. Here, we characterize the genome-wide distribution of 5hmC in T cells using DNA immunoprecipitation coupled with high-throughput DNA sequencing. 5hmC marks signature genes associated with effector cell differentiation in the putative regulatory elements. Moreover, Tet2 protein is recruited to 5hmC-containing regions, dependent on lineage-specific transcription factors. Deletion of the Tet2 gene in T cells decreased their cytokine expression, associated with reduced p300 recruitment. In vivo, Tet2 plays a critical role in the expression of cytokine genes. Collectively, our findings for the first time demonstrate a key role of Tet-mediated active DNA demethylation in T cells. A total of 8 samples were analyzed. The expression patterns in Tet2 wild-type and deficient Th1 and Th17 cells were analyzed.
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