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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE117920 | GEO | 2018/09/13

REPOSITORIES: GEO

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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

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

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

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