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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 [hMeDIP-seq]

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

2018-09-13 | GSE117919 | GEO

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

Hydroxylation of 5-methylcytosine by TET2 maintains the active state of the mammalian HOXA cluster

Project description:This SuperSeries is composed of the following subset Series: GSE32362: Hydroxylation of 5-methylcytosine by TET2 maintains the active state of the mammalian HOXA cluster (Illumina HumanMethylation450 BeadChip) GSE33129: Hydroxylation of 5-methylcytosine by TET2 maintains the active state of the mammalian HOXA cluster (Illumina HiSeq2000 sequencing) Refer to individual Series

2012-05-02 | E-GEOD-33130 | biostudies-arrayexpress

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

Chromatin-associated LTR RNA m5C oxidation by TET2 regulates chromatin state and leukemogenesis [seq_RNA-caRNA]

Project description:Mutation of Ten-eleven translocation enzyme 2 (TET2) drives myeloid malignancy initiation and progression. TET2 deficiency is known to cause a globally opened chromatin state and activation of genes contributing to aberrant hematopoietic stem cell self-renewal. However, the open chromatin observed in TET2-deficient mouse embryonic stem cells, leukemic cells and hematopoietic progenitor and stem cells is inconsistent with the designated role of DNA 5mC oxidation of TET2. We show here that chromatin-associated retrotransposon RNA 5-methylcytosine (m5C) can be recognized by the methyl-CpG-binding domain protein MBD6, which guides deubiquitination of nearby histone H2AK119ub to promote an open chromatin state. TET2 oxidizes m5C and antagonizes this MBD6-dependent H2AK119ub deubiquitination. Thereby, TET2 depletion leads to globally decreased H2AK119ub, more open chromatin, and increased transcription in stem cells. TET2 mutant human leukemia becomes dependent on this gene activation pathway, with MBD6 depletion selectively blocks proliferation of TET2 mutant leukemic cells and fully reverses the hematopoiesis defects caused by Tet2 loss, both in vitro and in vivo. Altogether, our findings reveal a chromatin regulation pathway by TET2 through retrotransposon RNA m5C oxidation and identify the downstream MBD6 protein as a feasible target for developing therapies specific against TET2 mutant malignancies.

2024-07-25 | GSE269961 | GEO

Chromatin-associated LTR RNA m5C oxidation by TET2 regulates chromatin state and leukemogenesis [seq_DNA-MeDIP]

2024-07-25 | GSE269960 | GEO

Chromatin-associated LTR RNA m5C oxidation by TET2 regulates chromatin state and leukemogenesis [seq_DNA-CUTandTag]

2024-07-25 | GSE269959 | GEO

Chromatin-associated LTR RNA m5C oxidation by TET2 regulates chromatin state and leukemogenesis [seq_DNA-ATAC_set2]

2024-07-25 | GSE269958 | 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

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