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Acetylation enhances TET2 function in protecting against abnormal DNA methylation during oxidative stress [gene expression]

ABSTRACT: Transcriptional profiling of A2780 cells with genetic TET2 knockout, generated by CRISPR. The aim was to identify genes affected by TET2 KO. Three individual KO clones were profiled. Control cells were cells that infected with control sgRNA.

ORGANISM(S): Homo sapiens

PROVIDER: GSE79808 | GEO | 2016/12/31

SECONDARY ACCESSION(S): PRJNA317022

REPOSITORIES: GEO

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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

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

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

Project description:Genome wide DNA methylation profiling of A2780 cells untreated (mock), treated with H2O2 for 30 min (H2O2 30 min), or treated with H2O2 for 30 min with additional 2.5 hour resting ( H2O2 3h) . 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 | GSE81426 | GEO

Acetylation enhances TET2 function in protecting against abnormal DNA methylation during oxidative stress [shTET2 - H2O2 - methylation]

Project description:Genome wide DNA methylation profilings (Bisulfite (BS), or oxidative bisulfite (oxBS)) were done for A2780 cells 1) infected with control virus, no H2O2 (Scr_mock) treatment, 2) infected with control virus with H2O2 treatment (30 min plus 2.5 h resting) (Scr_H2O2), and 3) infected with shTET2 virus, with H2O2 treatment (30 min plus 2.5 h resting) (shTET2_H2O2). Each genomic DNA was splitted equally to two aliquots. One aliquote was subjected to oxidation (oxBS) and one to mock oxidation (BS) prior to bisulfite treatment (CEGX protocol). The Illumina’s Infinium Human Methylation450 Beadchip Kit (WG-314-1001) was used to obtain DNA methylation profiles across approximately 450,000 CpGs. 5hmC levels were calculated by subtracting oxBS values from BS values.

2016-12-31 | GSE83750 | GEO

Acetylation enhances TET2 function in protecting against abnormal DNA methylation during oxidative stress [A2780 TET2KD damage 3h - methylation]

Project description:Genome wide DNA methylation profiling of A2780 cells 1) infected with control virus, no H2O2 (Scr_mock), 2) infected with control virus with H2O2 treatment (30 min plus 2.5 h resting) (Scr_H2O2), 3) infected with shTET2 virus, no H2O2 (shTET2_mock), and 4) infected with shTET2 virus, with H2O2 treatment (30 min plus 2.5 h resting) (shTET2_H2O2, two biological replicates). 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 | GSE81427 | GEO

Acetylation enhances TET2 function in protecting against abnormal DNA methylation during oxidative stress

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-12-31 | GSE81428 | GEO

Acetylation enhances TET2 function in protecting against abnormal DNA methylation during oxidative stress

Project description:Acetylation enhances TET2 function in protecting against abnormal DNA methylation during oxidative stress

| PRJNA321516 | ENA

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

TET2 deficiency promotes MDS-associated leukemogenesis

Project description:Loss of function TET2 mutations are frequently seen in myelodysplastic syndrome (MDS) patients. Previous studies have demonstrated that TET2 deficiency enhances maintenance of MDS hematopoietic stem and progenitor cells (HSPCs). Nonetheless, the pathogenic role of TET2 in MDS progression remains elusive. Here, we demonstrate Tet2 knockout (KO) markedly accelerated malignant transformation in Nup98-HoxD13 (NHD13) transgenic mice and promotes leukemogenesis of HoxA9 transduction/transplant mice. Consistently, low TET2 level cooperating with high HOXA9 level predicts poor outcome of MDS patients. Notably, Tet2 KO conferred a clonal advantage to the HSPCs of NHD13 mice. Whole-exome sequencing revealed that Tet2 KO facilitates accumulation of mutations at genes associated with leukemogenesis, including Arih2, whose loss of function promotes MDS cells proliferation. Using 5-hydroxymethylcytosine immunoprecipitation coupled with high-throughput sequencing analysis, we found while Tet2 deletion decreased overall 5hmC levels, it also increased 5hmC distribution at certain mutation loci such as Arih2. Vitamin C treatment, which mimics Tet2/Tet3 restoration, blocked disease progression in Tet2-deficient NHD13 mice. Collectively, our findings demonstrate that TET2 activity governs occurrence of secondary mutations in MDS HSPCs, providing a rationale for enhancing TETs function to block MDS-malignant transformation.

2022-10-12 | GSE213591 | GEO

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