ArticleProceedings of the National Academy of Sciences of the United States of America2021
Dnmt3a deficiency in the skin causes focal, canonical DNA hypomethylation and a cellular proliferation phenotype.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Overgrowth-intellectual disability disorders: progress in biology, patient advocacy and innovative therapies.Disease models & mechanisms · 2025Review
- DNA methylation in mammalian development and disease.Nature reviews. Genetics · 2025Review
- Melanoma in a patient with DNMT3A overgrowth syndrome.Cold Spring Harbor molecular case studies · 2023Article
- Functional compensation of mouse duplicates by their paralogs expressed in the same tissues.Genome biology and evolution · 2022Article
- A Hairy Cituation - PADIs in Regeneration and Alopecia.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
9 authors at 1 institution in 1 country.
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Abstract
DNA hypomethylation is a feature of epidermal cells from aged and sun-exposed skin, but the mechanisms responsible for this methylation loss are not known. Dnmt3a is the dominant de novo DNA methyltransferase in the skin; while epidermal Dnmt3a deficiency creates a premalignant state in which keratinocytes are more easily transformed by topical mutagens, the conditions responsible for this increased susceptibility to transformation are not well understood. Using whole genome bisulfite sequencing, we identified a focal, canonical DNA hypomethylation phenotype in the epidermal cells of Dnmt3a-deficient mice. Single-cell transcriptomic analysis revealed an increased proportion of cells with a proliferative gene expression signature, while other populations in the skin were relatively unchanged. Although total DNMT3A deficiency has not been described in human disease states, rare patients with an overgrowth syndrome associated with behavioral abnormalities and an increased risk of cancer often have heterozygous, germline mutations in
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