ArticleNature communications2022
Acute deletion of TET enzymes results in aneuploidy in mouse embryonic stem cells through decreased expression of Khdc3.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- TET Enzymes as Epigenetic Integrators in Intestinal Immunity, Inflammation, and Disease.Journal of personalized medicine · 2026Review
- 5-Hydroxymethylcytosine: a key epigenetic mark in cancer and chemotherapy response.Epigenetics & chromatin · 2025Review
- Mechanism of cytarabine-induced neurotoxicity.Nature · 2025Article
- Discrete genetic subtypes and tumor microenvironment signatures correlate with peripheral T-cell lymphoma outcomes.Leukemia · 2025Article
- A mutant ASXL1-BAP1-EHMT complex contributes to heterochromatin dysfunction in clonal hematopoiesis and chronic monomyelocytic leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Epigenetic crosstalk between stem cells and tumors: mechanisms and emerging perspectives.American journal of stem cells · 2025Review
- Potential role of miR-29b from mesenchymal stromal cell-derived extracellular vesicles in leukemic cell progression.PloS one · 2025Article
- Concomitant loss of TET2 and TET3 results in T cell expansion and genomic instability in mice.Communications biology · 2024Article
- Article
- TET Proteins in the Spotlight: Emerging Concepts of Epigenetic Regulation in T Cell Biology.ImmunoHorizons · 2023Article
- Epigenetic regulation in premature ovarian failure: A literature review.Frontiers in physiology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
TET (Ten-Eleven Translocation) dioxygenases effect DNA demethylation through successive oxidation of the methyl group of 5-methylcytosine (5mC) in DNA. In humans and in mouse models, TET loss-of-function has been linked to DNA damage, genome instability and oncogenesis. Here we show that acute deletion of all three Tet genes, after brief exposure of triple-floxed, Cre-ERT2-expressing mouse embryonic stem cells (mESC) to 4-hydroxytamoxifen, results in chromosome mis-segregation and aneuploidy; moreover, embryos lacking all three TET proteins showed striking variation in blastomere numbers and nuclear morphology at the 8-cell stage. Transcriptional profiling revealed that mRNA encoding a KH-domain protein, Khdc3 (Filia), was downregulated in triple TET-deficient mESC, concomitantly with increased methylation of CpG dinucleotides in the vicinity of the Khdc3 gene. Restoring KHDC3 levels in triple Tet-deficient mESC prevented aneuploidy. Thus, TET proteins regulate Khdc3 gene expression, and TET deficiency results in mitotic infidelity and genome instability in mESC at least partly through decreased expression of KHDC3.
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