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Mutations in human DNA methyltransferase DNMT1 induce specific genome-wide epigenomic and transcriptomic changes in neurodevelopment
Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Palo Alto, CA 94304 USA.;Stanford Univ, Sch Med, Dept Genet, Palo Alto, CA 94304 USA..
Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Palo Alto, CA 94304 USA.;Stanford Univ, Sch Med, Dept Genet, Palo Alto, CA 94304 USA..
Stanford Univ, Dept Stat, Stanford, CA 94305 USA..
Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Palo Alto, CA 94304 USA.;Stanford Univ, Sch Med, Ctr Narcolepsy, Palo Alto, CA 94304 USA..
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2023 (English)In: Human Molecular Genetics, ISSN 0964-6906, E-ISSN 1460-2083, Vol. 32, no 21, p. 3105-3120Article in journal (Refereed) Published
Abstract [en]

DNA methyltransferase type 1 (DNMT1) is a major enzyme involved in maintaining the methylation pattern after DNA replication. Mutations in DNMT1 have been associated with autosomal dominant cerebellar ataxia, deafness and narcolepsy (ADCA-DN). We used fibroblasts, induced pluripotent stem cells (iPSCs) and induced neurons (iNs) generated from patients with ADCA-DN and controls, to explore the epigenomic and transcriptomic effects of mutations in DNMT1. We show cell type–specific changes in gene expression and DNA methylation patterns. DNA methylation and gene expression changes were negatively correlated in iPSCs and iNs. In addition, we identified a group of genes associated with clinical phenotypes of ADCA-DN, including PDGFB and PRDM8 for cerebellar ataxia, psychosis and dementia and NR2F1 for deafness and optic atrophy. Furthermore, ZFP57, which is required to maintain gene imprinting through DNA methylation during early development, was hypomethylated in promoters and exhibited upregulated expression in patients with ADCA-DN in both iPSC and iNs. Our results provide insight into the functions of DNMT1 and the molecular changes associated with ADCA-DN, with potential implications for genes associated with related phenotypes.

Place, publisher, year, edition, pages
Oxford University Press, 2023. Vol. 32, no 21, p. 3105-3120
National Category
Cancer and Oncology Cell and Molecular Biology
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URN: urn:nbn:se:uu:diva-523252DOI: 10.1093/hmg/ddad123ISI: 001102978600007PubMedID: 37584462OAI: oai:DiVA.org:uu-523252DiVA, id: diva2:1838492
Funder
Swedish Research Council, 2020-01947The Swedish Brain Foundation, FO 2020-0171Available from: 2024-02-16 Created: 2024-02-16 Last updated: 2024-02-16Bibliographically approved

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Dahl, Niklas

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