ArticleCell reports2015
Haploinsufficiency, but not defective paternal 5mC oxidation, accounts for the developmental defects of maternal Tet3 knockouts.
Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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Who cites it
29 citing papers in PubMed, 46 citations in OpenAlex.
- Loss of Tet hydroxymethylase activity causes mouse embryonic stem cell differentiation bias and developmental defects.Science China. Life sciences · 2024Article
- Auto-suppression of Tet dioxygenases protects the mouse oocyte genome from oxidative demethylation.Nature structural & molecular biology · 2024Article
- TET enzyme driven epigenetic reprogramming in early embryos and its implication on long-term health.Frontiers in cell and developmental biology · 2024Review
- Review
- Mammalian DNA methylome dynamics: mechanisms, functions and new frontiers.Development (Cambridge, England) · 2022Review
- Early Expression of Tet1 and Tet2 in Mouse Zygotes Altered DNA Methylation Status and Affected Embryonic Development.International journal of molecular sciences · 2022Article
- Two families with TET3-related disorder showing neurodevelopmental delay with craniofacial dysmorphisms.Journal of human genetics · 2022Article
- Tet enzymes are essential for early embryogenesis and completion of embryonic genome activation.EMBO reports · 2022Article
- Maternal effect genes: Update and review of evidence for a link with birth defects.HGG advances · 2022Review
- Pathways of DNA Demethylation.Advances in experimental medicine and biology · 2022Article
- The preconception environment and sperm epigenetics.Andrology · 2020Review
- Delineation of a Human Mendelian Disorder of the DNA Demethylation Machinery: TET3 Deficiency.American journal of human genetics · 2020Article
- EHMT2 and SETDB1 protect the maternal pronucleus from 5mC oxidation.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Genomic insights into chromatin reprogramming to totipotency in embryos.The Journal of cell biology · 2019Review
- Somatic Cell Nuclear Transfer Reprogramming: Mechanisms and Applications.Cell stem cell · 2018Review
- Acquisition of oocyte competence to develop as an embryo: integrated nuclear and cytoplasmic events.Human reproduction update · 2018Review
- Embryonic defects induced by maternal obesity in mice derive from Stella insufficiency in oocytes.Nature genetics · 2018Article
- Developmental Functions of the Dynamic DNA Methylome and Hydroxymethylome in the Mouse and Zebrafish: Similarities and Differences.Frontiers in cell and developmental biology · 2018Review
- Epigenetic Regulations in Neural Stem Cells and Neurological Diseases.Stem cells international · 2018Review
- A Lexicon of DNA Modifications: Their Roles in Embryo Development and the Germline.Frontiers in cell and developmental biology · 2018Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Paternal DNA demethylation in mammalian zygotes is achieved through Tet3-mediated iterative oxidation of 5-methylcytosine (5mC) coupled with replication-dependent dilution. Tet3-mediated paternal DNA demethylation is believed to play important roles in mouse development given that Tet3 heterozygous embryos derived from Tet3-deficient oocytes exhibit embryonic sublethality. Here, we demonstrate that the sublethality phenotype of the Tet3 maternal knockout mice is caused by haploinsufficiency but not defective paternal 5mC oxidation. We found that Tet3 heterozygous progenies derived from heterozygous father or mother also exhibit sublethality. Importantly, wild-type embryos reconstituted with paternal pronuclei that bypassed 5mC oxidation develop and grow to adulthood normally. Genome-scale DNA methylation analysis demonstrated that hypermethylation in maternal Tet3 knockout embryos is largely diminished by the blastocyst stage. Our study thus reveals that Tet3-mediated paternal 5mC oxidation is dispensable for mouse development and suggests the existence of a compensatory mechanism for defective 5mC oxidation in preimplantation embryos.
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Registered trials
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.