ArticleScientific reports2015
Maternal TET3 is dispensable for embryonic development but is required for neonatal growth.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed.
- TET knockout cells transit between pluripotent states and exhibit precocious germline entry.The EMBO journal · 2025Article
- Article
- TET3-facilitated differentiation of human umbilical cord mesenchymal stem cells into oligodendrocyte precursor cells for spinal cord injury recovery.Journal of translational medicine · 2024Article
- Iterative oxidation by TET1 is required for reprogramming of imprinting control regions and patterning of mouse sperm hypomethylated regions.Developmental cell · 2024Article
- Catalytic-dependent and -independent roles of TET3 in the regulation of specific genetic programs during neuroectoderm specification.Communications biology · 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
- TET Family Members Are Integral to Porcine Oocyte Maturation and Parthenogenetic Pre-Implantation Embryogenesis.International journal of molecular sciences · 2023Article
- Deficiency of Tet3 in nucleus accumbens enhances fear generalization and anxiety-like behaviors in mice.Brain pathology (Zurich, Switzerland) · 2022Article
- Increased mtDNA mutation frequency in oocytes causes epigenetic alterations and embryonic defects.National science review · 2022Article
- Role of DNA dioxygenase Ten-Eleven translocation 3 (TET3) in rheumatoid arthritis progression.Arthritis research & therapy · 2022Article
- Early Expression of Tet1 and Tet2 in Mouse Zygotes Altered DNA Methylation Status and Affected Embryonic Development.International journal of molecular sciences · 2022Article
- Article
- Maternal effect factors that contribute to oocytes developmental competence: an update.Journal of assisted reproduction and genetics · 2022Review
- Two families with TET3-related disorder showing neurodevelopmental delay with craniofacial dysmorphisms.Journal of human genetics · 2022Article
- The Epigenetic Role of Vitamin C in Neurodevelopment.International journal of molecular sciences · 2022Review
- 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
- Asymmetrical deposition and modification of histone H3 variants are essential for zygote development.Life science alliance · 2021Article
- Totipotency of mouse zygotes extends to single blastomeres of embryos at the four-cell stage.Scientific reports · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development of multicellular organisms is accompanied by reprogramming of the epigenome in specific cells, with the epigenome of most cell types becoming fixed after differentiation. Genome-wide reprogramming of DNA methylation occurs in primordial germ cells and in fertilized eggs during mammalian embryogenesis. The 5-methylcytosine (5mC) content of DNA thus undergoes a marked decrease in the paternal pronucleus of mammalian zygotes. This loss of DNA methylation has been thought to be mediated by an active demethylation mechanism independent of replication and to be required for development. TET3-mediated sequential oxidation of 5mC has recently been shown to contribute to the genome-wide loss of 5mC in the paternal pronucleus of mouse zygotes. We now show that TET3 localizes not only to the paternal pronucleus but also to the maternal pronucleus and oxidizes both paternal and maternal DNA in mouse zygotes, although these phenomena are less pronounced in the female pronucleus. Genetic ablation of TET3 in oocytes had no significant effect on oocyte development, maturation, or fertilization or on pregnancy, but it resulted in neonatal sublethality. Our results thus indicate that zygotic 5mC oxidation mediated by maternal TET3 is required for neonatal growth but is not essential for development.
Indexed as
Identifiers
What OpenQuestion holds
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.