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DNA methylation (5-methylcytosine (5mC)) is critical for genome stability and transcriptional regulation in mammals. The discovery that ten-eleven translocation (TET) proteins catalyze the oxidation of 5mC to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), and 5-carboxylcytosine (5caC) revolutionized our perspective on the complexity and regulation of DNA modifications. However, to what extent the regulatory functions of TET1 can be attributed to its catalytic activity remains unclear. Here, we use genome engineering and quantitative multi-omics approaches to dissect the precise catalytic vs. non-catalytic functions of TET1 in murine embryonic stem cells (mESCs). Our study identifies TET1 as an essential interaction hub for multiple chromatin modifying complexes and a global regulator of histone modifications. Strikingly, we find that the majority of transcriptional regulation depends on non-catalytic functions of TET1. In particular, we show that TET1 is critical for the establishment of H3K9me3 and H4K20me3 at endogenous retroviral elements (ERVs) and their silencing that is independent of its canonical role in DNA demethylation. Furthermore, we provide evidence that this repression of ERVs 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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http://dx.doi.org/10.1093/nar/gkac642 | DOI Listing |
Adv Biomed Res
November 2024
Department of Cellular and Molecular Nutrition, Faculty of Nutrition Science and Food Technology, National Nutrition and Food Technology Research Institute, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Background: Acquisition of stem-like properties requires overcoming the epigenetic barrier of differentiation and re-expression of several genes involved in stemness and the cell cycle. DNA methylation is the classic epigenetic mechanism for de/differentiation. The writers and erasers of DNA methylation are not site-specific enzymes for altering specific gene methylation.
View Article and Find Full Text PDFInt J Pharm
December 2024
Biochemistry Department, Faculty of Science, Alexandria University, Alexandria 21511, Egypt. Electronic address:
Nat Commun
November 2024
McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA, USA.
Epigenomics
December 2024
Department of Epigenetics, Van Andel Institute, Grand Rapids, MI, USA.
Aims: Mammalian genomes encode 12 proteins that contain a CXXC zinc finger domain. Most members of this family are large multi-domain proteins that function in the control of DNA methylation and histone methylation patterns. CXXC5 is a smaller member of the family, along with its closest homologue CXXC4.
View Article and Find Full Text PDFGenes Dev
November 2024
Division of Molecular, Cellular, and Developmental Biology, University of Dundee, Dundee DD1 5EH, United Kingdom;
The link between DNA methylation and neurodevelopmental disorders is well established. However, how DNA methylation is fine-tuned-ensuring precise gene expression and developmental fidelity-remains poorly understood. PROSER1, a known TET2 interactor, was recently linked to a severe neurodevelopmental disorder.
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