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Tet2 orchestrates dynamics of hydroxy-methylation and chromatin state during cell reprogramming [ATAC-seq]

ABSTRACT: Tet2 orchestrates dynamics of hydroxy-methylation and chromatin state during cell reprogramming [ATAC-seq]

PROVIDER: PRJNA483740 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7628230_1.fastq.gz	Fastqsanger.gz
	SRR7628230_2.fastq.gz	Fastqsanger.gz
	SRR7628231_1.fastq.gz	Fastqsanger.gz
	SRR7628231_2.fastq.gz	Fastqsanger.gz
	SRR7628232_1.fastq.gz	Fastqsanger.gz

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Tet2 orchestrates dynamics of hydroxy-methylation and chromatin state during cell reprogramming [hMeDIP-seq]

Project description:Tet2 orchestrates dynamics of hydroxy-methylation and chromatin state during cell reprogramming [hMeDIP-seq]

| PRJNA483742 | ENA

Tet2 orchestrates dynamics of hydroxy-methylation and chromatin state during cell reprogramming [ATAC-seq]

Project description:Studies of DNA hydroxy-methylation and chromatin state dynamics during highly-efficient somatic cell reprogramming

2018-09-13 | GSE117920 | GEO

Tet2 orchestrates dynamics of hydroxy-methylation and chromatin state during cell reprogramming [hMeDIP-seq]

Project description:Studies of DNA hydroxy-methylation and chromatin state dynamics during highly-efficient somatic cell reprogramming

2018-09-13 | GSE117919 | GEO

TET1-mediated DNA hydroxy-methylation regulates adult remyelination

Project description:Adult myelination is essential for brain function and response to injury, but the molecular mechanisms remain elusive. Here we identify DNA hydroxy-methylation, an epigenetic mark catalyzed by Ten-Eleven translocation (TET) enzymes, as necessary for adult myelin repair. While DNA hydroxy-methylation and high levels of TET1 were detected in young adult mice during myelin regeneration after demyelination, this process was defective in old mice. Constitutive or inducible lineage-specific ablation of Tet1 (but not of Tet2) recapitulated the age-related decline of DNA hydroxy-methylation and inefficient remyelination. Genome-wide hydroxy-methylation and transcriptomic analysis identified solute carrier gene families as TET1 targets. Lower transcripts for these genes in Tet1 mutants and old mice were associated with swelling at the neuroglial interface, a phenotype detected also in zebrafish Slc12a2b mutants. We conclude that TET1-mediated DNA hydroxy-methylation is necessary for adult myelination after injury, by modulating the levels of the solute carrier SLC12A2 at the axo-myelin interface.

2020-03-14 | GSE137611 | GEO

Age-dependent decline of TET1-mediated DNA hydroxy-methylation impairs myelin regeneration after injury

Project description:Adult myelination is recognized as essential for brain function and response to injury and yet, its molecular understanding is mostly inferred from developmental studies. In this study, we identify DNA hydroxy-methylation, an epigenetic mark catalyzed by Ten-Eleven translocation (TET) enzymes, as necessary for adult, but not for developmental, myelin formation. While hydroxy-methylation and high levels of TET1 were detected in young adult mice during myelin regeneration after lysolecithin-induced demyelination, this process was defective in older mice. Lineage specific ablation of the enzyme Tet1 (but not of Tet2) recapitulated the age-related decline of TET1 and inefficient remyelination, without impacting developmental myelination. Genome-wide DNA hydroxy-methylation profiling of adult progenitors and mature oligodendrocytes, identified solute carriers regulating neuronal-glial communication as gene targets, whose expression was dramatically decreased in mutants and in older mice. We conclude that TET1-mediated hydroxy-methylation is critical for adult myelination in response to injury.

2020-03-14 | GSE122446 | GEO

SETDB1 Orchestrates Metabolic Reprogramming to Regulate Cell State Maintenance and Cell Fate Differentiation

Project description:SETDB1 Orchestrates Metabolic Reprogramming to Regulate Cell State Maintenance and Cell Fate Differentiation

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DNA hydroxy-methylation data of tumor and non-tumor liver (NTL) tissues from Peruvian patients with hepatocellular carcinoma (HCC)

Project description:A large fraction of HCC in Peru arises in younger, non-cirrhotic patients. Global DNA hydroxy-methylation analysis of the HCC and NTL tissues demonstrate that hydroxy-methylation conversion interplays with gene expression to enact cell fate determination and cancer cell reprogramming. We used microarrays to identify hydroxy-methylated CpGs by comparison to Gene Expression Omnibus (GEO) series GSE136319 and GSE136380.

2021-01-31 | GSE136583 | GEO

14-3-3 protects AMPK phosphorylated TET2 from dephosphorylation by PP2A

Project description:Ten-eleven translocation-2 (TET2) is a member of the methylcytosine dioxygenase family of enzymes implicated in cancer and in aging due to its role as a global epigenetic modifier. TET2 has a large N-terminal domain followed by a catalytic C-terminal. Previous reports have demonstrated that the catalytic domain remains active independent of the N-terminal domain. As such, the function of the N-terminus of this large protein remains poorly characterized. Here, we identify that several isoforms of the 14-3-3 family of proteins bind TET2. 14-3-3s bind TET2 when phosphorylated at serine 99 (S99). AMPK-mediated phosphorylation at S99 promotes TET2 stability and increases global DNA 5-hydroxymethylcytosine. 14-3-3s’ interaction with TET2 serves to protect S99 phosphorylation. Disruption of this interaction leads to both reduced TET2 phosphorylation and decreased protein stability. Furthermore, we identify that the protein phosphatase 2A (PP2A) can interact with TET2 and dephosphorylates S99. Collectively, our study provides novel insights into the role of the N-terminal domain in TET2 regulation. Moreover, they demonstrate the dynamic nature of TET2 protein regulation that could have therapeutic implications for disease states resulting from reduced TET2 levels and/or activity.

2020-01-13 | PXD016160 | Pride

Distinct roles of Tet1 and Tet2 in mouse embryonic stem cells (CMS-Seq)

Project description:The TET proteins TET1, TET2 and TET3 constitute a new family of dioxygenases that utilize molecular oxygen and the cofactors Fe(II) and 2-oxoglutarate to convert 5-methylcytosine (5mC) to 5-hydroxy-methylcytosine (5hmC) and further oxidation products in DNA1-5. Here we show that Tet1 and Tet2 have distinct roles in regulating 5hmC deposition and gene expression in mouse embryonic stem cells (mESC). Tet1 depletion in mESC primarily diminishes 5hmC levels at transcription start sites (TSS), whereas Tet2 depletion is mostly associated with decreased 5hmC in gene bodies relative to TSS. 5hmC is enriched at exon start and end sites, especially in exons that are highly expressed, and is significantly decreased upon Tet2 knockdown at the boundaries of high-expressed exons that are selectively regulated by Tet2. In differentiating murine B cells, Tet2 deficiency is associated with selective exon exclusion in the gene encoding the transmembrane phosphatase CD45. Tet2 depletion is associated with increased 5hmC and decreased 5mC at promoters/ TSS regions, possibly because of the redundant activity of Tet1. Together, these data indicate a complex interplay between Tet1 and Tet2 in mESC, and show that loss-of-function of a single TET protein does not necessarily lead to loss of 5hmC and a corresponding gain of 5mC, as generally assumed. The relation between Tet2 loss-of-function and selective changes in exon expression could potentially explain the frequent occurrence of both TET2 loss-of-function mutations and mutations in proteins involved in pre-mRNA splicing in myeloid malignancies in humans. Gene and exon expression analysis in mESC, Tet1 knockdown mESC, and Tet2 knockdown mESC by RNA-sequencing. Mapping of 5-hydroxymethylcytosine in mESC, Tet1 knockdown mESC, and Tet2 knockdown mESC by anti-CMS-seq. Mapping of methylcytosine in mESC, and Tet2 kd mESC by MeDIP-seq.

2014-01-16 | E-GEOD-50200 | biostudies-arrayexpress

Distinct roles of Tet1 and Tet2 in mouse embryonic stem cells (RNA-Seq)

2014-01-16 | E-GEOD-50198 | biostudies-arrayexpress