ArticleNucleic acids research2022
TET1 regulates gene expression and repression of endogenous retroviruses independent of DNA demethylation.
Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 43 citations in OpenAlex.
- Rare protein-coding variation and the genetic architecture of height in >1.4 million individuals.medRxiv : the preprint server for health sciences · 2026Article
- Intrinsic regulation of intestinal stem cell fate and homeostasis by Tet.bioRxiv : the preprint server for biology · 2026Article
- Epigenetic editing: from concept to clinic.Nature reviews. Drug discovery · 2026Review
- RETRACTED: Endogenous Retroviruses as Regulators of Innate Immune Signaling and InflammationViruses · 2026Review
- Epigenetic regulation of PANoptosis: DNA methylation, histone modifications and non-coding RNAs.EXCLI journal · 2026Review
- Catalytic-independent roles of chromatin modifiers in mammalian development and the implications for treating human disease.Biochemical Society transactions · 2025Review
- TET knockout cells transit between pluripotent states and exhibit precocious germline entry.The EMBO journal · 2025Article
- TET dioxygenases localize at splicing speckles and promote RNA splicing.Nucleus (Austin, Tex.) · 2025Article
- Endogenous Retroviruses in Host-Virus Coevolution: From Genomic Domestication to Functional Innovation.Genes · 2025Review
- Maternal Vitamin C Deficiency and Genetic Risk Factors Contribute to Congenital Defects through Dysregulation of DNA Methylation.bioRxiv : the preprint server for biology · 2025Article
- Decoding the epigenetic and transcriptional basis of direct cardiac reprogramming.Stem cells (Dayton, Ohio) · 2025Review
- Multiplexed chromatin immunoprecipitation sequencing for quantitative study of histone modifications and chromatin factors.Nature protocols · 2025Review
- SilencingEnvironmental epigenetics · 2025Article
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- Loss of Tet hydroxymethylase activity causes mouse embryonic stem cell differentiation bias and developmental defects.Science China. Life sciences · 2024Article
- Memory effects of prior subculture may impact the quality of multiomic perturbation profiles.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Genome-wide 5-hydroxymethylcytosines in circulating cell-free DNA as noninvasive diagnostic markers for gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2024Article
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- Niche Tet maintains germline stem cells independently of dioxygenase activity.The EMBO journal · 2024Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.