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Tet1 and Tet2 mediate epigenetic regulation of developmental genes by protecting DNA methylation canyons against hypermethylation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE58611 | GEO | 2015/12/07

SECONDARY ACCESSION(S): PRJNA253009

REPOSITORIES: GEO

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Tet1 and Tet2 mediate epigenetic regulation of developmental genes by protecting DNA methylation canyons against hypermethylation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-12-07 | E-GEOD-58611 | biostudies-arrayexpress

Tet1 and Tet2 mediate epigenetic regulation of developmental genes by protecting DNA methylation canyons against hypermethylation [RNA-Seq]

Project description:This study uses whole-transcriptome sequencing to characterize the transcriptomes of mouse embryonic fibroblasts (MEF's). Two conditions were analyzed, MEF cells with intact TET1/TET2 enzymes (WT) and MEF cells with TET1/TET2 knocked out (DKO). Our results identify sets of differentially expressed genes which are correlated with TET1/TET2 induced methylation changes of the corresponding genes. Whole transcriptome analysis of M. musculus MEF cells. Two conditions were sequenced and analyzed, the first is wild type (WT), the second corresponds to knock-out of TET1 and TET2 enzymes.

2015-12-07 | E-GEOD-58609 | biostudies-arrayexpress

Tet1 and Tet2 mediate epigenetic regulation of developmental genes by protecting DNA methylation canyons against hypermethylation [Bisulfite-Seq]

Project description:This study uses whole methylome sequencing to characterize the methylomes of mouse embryonic fibroblasts (MEF's). Two conditions were analyzed, MEF cells with intact TET1/TET2 enzymes (WT) and MEF cells with TET1/TET2 knocked out (DKO). Our results identify sets of differentially methylated genes which are correlated with TET1/TET2 induced expression changes of the corresponding genes. Whole methylome analysis of M. musculus MEF cells. Two conditions were sequenced and analyzed, the first is wild type (WT), the second (DKO) corresponds to knock-out of TET1 and TET2 enzymes.

2015-12-07 | E-GEOD-58610 | biostudies-arrayexpress

Tet1 and Tet2 mediate epigenetic regulation of developmental genes by protecting DNA methylation canyons against hypermethylation [Bisulfite-Seq]

2015-12-07 | GSE58610 | GEO

Tet1 and Tet2 mediate epigenetic regulation of developmental genes by protecting DNA methylation canyons against hypermethylation [RNA-Seq]

2015-12-07 | GSE58609 | GEO

Tet1 and Tet2 Protect DNA Methylation Canyons against Hypermethylation.

Project description:DNA methylation is a dynamic epigenetic modification with an important role in cell fate specification and reprogramming. The Ten eleven translocation (Tet) family of enzymes converts 5-methylcytosine to 5-hydroxymethylcytosine, which promotes passive DNA demethylation and functions as an intermediate in an active DNA demethylation process. Tet1/Tet2 double-knockout mice are characterized by developmental defects and epigenetic instability, suggesting a requirement for Tet-mediated DNA demethylation for the proper regulation of gene expression during differentiation. Here, we used whole-genome bisulfite and transcriptome sequencing to characterize the underlying mechanisms. Our results uncover the hypermethylation of DNA methylation canyons as the genomic key feature of Tet1/Tet2 double-knockout mouse embryonic fibroblasts. Canyon hypermethylation coincided with disturbed regulation of associated genes, suggesting a mechanistic explanation for the observed Tet-dependent differentiation defects. Based on these results, we propose an important regulatory role of Tet-dependent DNA demethylation for the maintenance of DNA methylation canyons, which prevents invasive DNA methylation and allows functional regulation of canyon-associated genes.

| S-EPMC4719427 | biostudies-literature

Tet1 and Tet2 mediate epigenetic regulation of developmental genes by protecting DNA methylation canyons against hypermethylation

Project description:Tet1 and Tet2 mediate epigenetic regulation of developmental genes by protecting DNA methylation canyons against hypermethylation

| PRJNA253009 | ENA

Acetylation Enhances TET2 Function in Protecting against Abnormal DNA Methylation during Oxidative Stress.

Project description:TET proteins, by converting 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), are hypothesized, but not directly shown, to protect promoter CpG islands (CGIs) against abnormal DNA methylation (DNAm) in cancer. We define such a protective role linked to DNA damage from oxidative stress (OS) known to induce this abnormality. TET2 removes aberrant DNAm during OS through interacting with DNA methyltransferases (DNMTs) in a "Yin-Yang" complex targeted to chromatin and enhanced by p300 mediated TET2 acetylation. Abnormal gains of DNAm and 5hmC occur simultaneously in OS, and knocking down TET2 dynamically alters this balance by enhancing 5mC and reducing 5hmC. TET2 reduction results in hypermethylation of promoter CGIs and enhancers in loci largely overlapping with those induced by OS. Thus, TET2 indeed may protect against abnormal, cancer DNAm in a manner linked to DNA damage.

| S-EPMC5260804 | biostudies-literature

miR-543 regulates the epigenetic landscape of myelofibrosis by targeting TET1 and TET2.

Project description:Myelofibrosis (MF) is a myeloproliferative neoplasm characterized by cytopenia and extramedullary hematopoiesis, resulting in splenomegaly. Multiple pathological mechanisms (e.g., circulating cytokines and genetic alterations, such as JAKV617F mutation) have been implicated in the etiology of MF, but the molecular mechanism causing resistance to JAK2V617F inhibitor therapy remains unknown. Among MF patients who were treated with the JAK inhibitor ruxolitinib, we compared noncoding RNA profiles of ruxolitinib therapy responders versus nonresponders and found miR-543 was significantly upregulated in nonresponders. We validated these findings by reverse transcription-quantitative PCR. in this same cohort, in 2 additional independent MF patient cohorts from the United States and Romania, and in a JAK2V617F mouse model of MF. Both in vitro and in vivo models were used to determine the underlying molecular mechanism of miR-543 in MF. Here, we demonstrate that miR-543 targets the dioxygenases ten-eleven translocation 1 (TET1) and 2 (TET2) in patients and in vitro, causing increased levels of global 5-methylcytosine, while decreasing the acetylation of histone 3, STAT3, and tumor protein p53. Mechanistically, we found that activation of STAT3 by JAKs epigenetically controls miR-543 expression via binding the promoter region of miR-543. Furthermore, miR-543 upregulation promotes the expression of genes related to drug metabolism, including CYP3A4, which is involved in ruxolitinib metabolism. Our findings suggest miR-543 as a potentially novel biomarker for the prognosis of MF patients with a high risk of treatment resistance and as a potentially new target for the development of new treatment options.

| S-EPMC7030823 | biostudies-literature

Acetylation enhances TET2 function in protecting against abnormal DNA methylation during oxidative stress [A2780 TET2 KO - methylation]

Project description:Genome wide DNA methylation profiling of A2780 control cells (Scr_1 and Scr_2), and A2780 TET2 KO clones (KO1.1, KO1.36, and KO2.32). The Illumina’s Infinium Human Methylation450 Beadchip Kit (WG-314-1001) was used to obtain DNA methylation profiles across approximately 450,000 CpGs.

2016-12-31 | GSE83751 | GEO

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