ArticlePLoS genetics2021
The DNMT3A PWWP domain is essential for the normal DNA methylation landscape in mouse somatic cells and oocytes.
Article in PLoS genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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21 citing papers in PubMed, 56 citations in OpenAlex.
- A progeria syndrome links DNA hypermethylation to age-related pathology.Nature genetics · 2026Article
- Mechanisms of DNA methyltransferase 3A1-mediated DNA methylation of nucleosomes.The Journal of biological chemistry · 2026Article
- Mono-ubiquitination of histone H2A lysine 119 (H2AK119Ub): its multifaceted role in biology and implication in diseases.MedScience · 2026Review
- Role of epigenetic regulation in diminished ovarian reserve.Journal of assisted reproduction and genetics · 2025Review
- Transcriptome and DNA methylation profiling during the NSN to SN transition in mouse oocytes.BMC molecular and cell biology · 2025Article
- Article
- The N-terminal region of DNMT3A engages the nucleosome surface to aid chromatin recruitment.EMBO reports · 2024Article
- Cancer-associated DNA hypermethylation of Polycomb targets requires DNMT3A dual recognition of histone H2AK119 ubiquitination and the nucleosome acidic patch.Science advances · 2024Article
- Specific DNMT3C flanking sequence preferences facilitate methylation of young murine retrotransposons.Communications biology · 2024Article
- Combined and differential roles of ADD domains of DNMT3A and DNMT3L on DNA methylation landscapes in mouse germ cells.Nature communications · 2024Article
- Roles of endogenous retroviral elements in the establishment and maintenance of imprinted gene expression.Frontiers in cell and developmental biology · 2024Review
- Article
- Expression analysis suggests that DNMT3L is required for oocyte de novo DNA methylation only in Muridae and Cricetidae rodents.Epigenetics & chromatin · 2023Article
- The DNMT3A ADD domain is required for efficient de novo DNA methylation and maternal imprinting in mouse oocytes.PLoS genetics · 2023Article
- Base editor scanning charts the DNMT3A activity landscape.Nature chemical biology · 2023Article
- CMIC: predicting DNA methylation inheritance of CpG islands with embedding vectors of variable-length k-mers.BMC bioinformatics · 2022Article
- Histone H3K36me2 and H3K36me3 form a chromatin platform essential for DNMT3A-dependent DNA methylation in mouse oocytes.Nature communications · 2022Article
- KDM4C Contributes to Trophoblast-like Stem Cell Conversion from Porcine-Induced Pluripotent Stem Cells (piPSCs) via Regulating CDX2.International journal of molecular sciences · 2022Article
- Comparative transcriptome analysis of heat-induced domesticated zebrafish during gonadal differentiation.BMC genomic data · 2022Article
- Genetic Studies on Mammalian DNA Methyltransferases.Advances in experimental medicine and biology · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA methylation at CG sites is important for gene regulation and embryonic development. In mouse oocytes, de novo CG methylation requires preceding transcription-coupled histone mark H3K36me3 and is mediated by a DNA methyltransferase DNMT3A. DNMT3A has a PWWP domain, which recognizes H3K36me2/3, and heterozygous mutations in this domain, including D329A substitution, cause aberrant CG hypermethylation of regions marked by H3K27me3 in somatic cells, leading to a dwarfism phenotype. We herein demonstrate that D329A homozygous mice show greater CG hypermethylation and severer dwarfism. In oocytes, D329A substitution did not affect CG methylation of H3K36me2/3-marked regions, including maternally methylated imprinting control regions; rather, it caused aberrant hypermethylation in regions lacking H3K36me2/3, including H3K27me3-marked regions. Thus, the role of the PWWP domain in CG methylation seems similar in somatic cells and oocytes; however, there were cell-type-specific differences in affected regions. The major satellite repeat was also hypermethylated in mutant oocytes. Contrary to the CA hypomethylation in somatic cells, the mutation caused hypermethylation at CH sites, including CA sites. Surprisingly, oocytes expressing only the mutated protein could support embryonic and postnatal development. Our study reveals that the DNMT3A PWWP domain is important for suppressing aberrant CG hypermethylation in both somatic cells and oocytes but that D329A mutation has little impact on the developmental potential of oocytes.
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