ArticleNucleic acids research2019
DNMT3B shapes the mCA landscape and regulates mCG for promoter bivalency in human embryonic stem cells.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Non-CG DNA methylation in animal genomes.Nature genetics · 2025Review
- Chromatin modifiers in neurodevelopment.Frontiers in molecular neuroscience · 2025Review
- Uncovering the roles of DNA hemi-methylation in transcriptional regulation using MspJI-assisted hemi-methylation sequencing.Nucleic acids research · 2024Article
- Embryonic Stem Cell-Derived Neurons as a Model System for Epigenome Maturation during Development.Genes · 2023Article
- The aberrant epigenome ofGenome research · 2023Article
- Non-coding RNA LEVER sequestration of PRC2 can mediate long range gene regulation.Communications biology · 2022Article
- Reciprocal epigenetic remodeling controls testicular cancer hypersensitivity to hypomethylating agents and chemotherapy.Molecular oncology · 2022Article
- Proteins in DNA methylation and their role in neural stem cell proliferation and differentiation.Cell regeneration (London, England) · 2021Review
- ZNF143 mediates CTCF-bound promoter-enhancer loops required for murine hematopoietic stem and progenitor cell function.Nature communications · 2021Article
- Complex DNA sequence readout mechanisms of the DNMT3B DNA methyltransferase.Nucleic acids research · 2020Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
DNMT3B is known as a de novo DNA methyltransferase. However, its preferential target sites for DNA methylation are largely unknown. Our analysis on ChIP-seq experiment in human embryonic stem cells (hESC) revealed that DNMT3B, mCA and H3K36me3 share the same genomic distribution profile. Deletion of DNMT3B or its histone-interacting domain (PWWP) demolished mCA in hESCs, suggesting that PWWP domain of DNMT3B directs the formation of mCA landscape. In contrast to the common presumption that PWWP guides DNMT3B-mediated mCG deposition, we found that deleting PWWP does not affect the mCG landscape. Nonetheless, DNMT3B knockout led to the formation of 2985 de novo hypomethylated regions at annotated promoter sites. Upon knockout, most of these promoters gain the bivalent marks, H3K4me3 and H3K27me3. We call them spurious bivalent promoters. Gene ontology analysis associated spurious bivalent promoters with development and cell differentiation. Overall, we found the importance of DNMT3B for shaping the mCA landscape and for maintaining the fidelity of the bivalent promoters in hESCs.
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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.