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Effect of TET1 overexpression on DNA methylation levels of HEK293 cells

ABSTRACT: We compared TET1 overexpressing cells to uninduced cells with endogenous TET1 transcript levels to determine DNA methylation changes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE67349 | GEO | 2015/07/16

SECONDARY ACCESSION(S): PRJNA279567

REPOSITORIES: GEO

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Effect of TET1 overexpression on hydroxymethylcytosine levels of HEK293 cells

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Effect of TET1 overexpression on DNA methylation levels of HEK293 cells

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Project description:Precise regulation of DNA methylation in mammals is critical for genome stability and epigenetic regulation. The discovery of the ten-eleven translocation (TET) proteins catalyzing the oxidation from 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), and 5-carboxylcytosine (5caC) revolutionized the perspective on the complexity and regulation of DNA modifications. Despite accumulating knowledge about the role of TET1, it remains unclear to what extent these can be attributed to its catalytic activity. Here, we use genome engineering and quantitative multi-omics approaches to dissect the role and mechanism of TET1 in mESCs. Our study identifies TET1 as an essential interaction hub for multiple chromatin modifying complexes and as a global regulator of histone modifications. Strikingly, we find that the majority of transcriptional regulation depends on non-catalytic functions of TET1. Moreover, we show that the establishment of H3K9me3 and H4K20me3 at ERV1, ERVK, and ERVL is mediated by TET1 independent of DNA demethylation. We provide evidence that repression of endogenous retroviruses depends on the interaction between TET1 and SIN3A. In summary, we demonstrate that the non-catalytic functions of TET1 are critical for regulation of gene expression and the silencing of endogenous retroviruses in mESCs.

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