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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE117919 | GEO | 2018/09/13

REPOSITORIES: GEO

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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

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

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

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Transcription factors drive Tet2-mediated enhancer demethylation to reprogram cell fate [Bisulfite-Seq]

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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

LJMJDW: Cellular responses to 4-hydroxy-2-nonenal

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Early N-hydroxy-pipecolic acid transcriptional profile

Project description:Early N-hydroxy-pipecolic acid transcriptional profile

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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.

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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

H3K4 Methylation-Mediated Memory of an Active Transcriptional State Impairs Nuclear Reprogramming

Project description:Xenopus eggs can induce the reversal of differentiation processes of somatic cells. Yet, the egg is not fully efficient in reprogramming a differentiated nucleus, as certain genes retain a memory of gene expression of their somatic cell of origin. This is thought to be a reason for the low success rate of current cloning and reprogramming strategies. While previous studies addressed extensively the mechanisms that maintain an inactive state of genes (OFF-memory), we investigated the importance of memory of an active transcriptional state (ON-memory) in maintaining cell fate identity and on resistance to reprogramming. We find that donor cell-type specific ON-memory gene-expression in the wrong cell-type of nuclear transfer (NT)-embryos is as common as OFF-memory gene-expression. When compared to properly reprogrammed genes, we find that ON-memory genes show an elevated level of the active histone mark H3K4me3 in endoderm donor cells. Importantly, we show that a reduction of H3K4 methylation level in donor cells decreases the extent of ON-memory gene expression, globally improves transcriptional reprogramming, and enhances the development of NT-embryos. Therefore, our study reveals that H3K4 methylation safeguards endoderm cell identity and acts as a major barrier for efficient reprogramming in NT-embryos. Furthermore, our results suggest that efficient cell fate reprogramming not only relies on the erasure of epigenetic modifications conferring OFF-memory but also crucially depends on the removal of H3 lysine 4 methylation-mediated memory of an active state of gene expression.

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