ArticleNature communications2016
Writing of H3K4Me3 overcomes epigenetic silencing in a sustained but context-dependent manner.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers.
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Who cites it
146 citing papers in PubMed.
- From epigenetic mark detection to rational design of epigenetic editing strategies.Molecular therapy. Advances · 2026Review
- Nuclear class 3 PI3K co-activates fasting-specific chromatin remodelling.Nature cell biology · 2026Article
- Designing and testing CRISPRi-based synthetic gene circuits in plants.Nature protocols · 2026Review
- Advances and clinical potential of epigenome editing.Cellular and molecular life sciences : CMLS · 2026Review
- Hierarchical interplay between H3K27ac and H3K4me3 in transcriptional regulation.Nature communications · 2026Article
- Trans-histone crosstalk establishes distinct H3K79 methylation zones with differential transcriptional functions.Nucleic acids research · 2026Article
- Modifying meiotic recombination by targeting chromatin regulators to crossover hotspots inScience advances · 2026Article
- Epigenetic editing: from concept to clinic.Nature reviews. Drug discovery · 2026Review
- Epigenome editing based treatment: Progresses and challenges.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Review
- Set1-dependent H3K4 methylation is essential for sustained gene expression at newly activated loci.Molecules and cells · 2026Article
- CRISPR-based Transcriptional Regulation: Technologies, Applications, and Future Directions.DNA · 2025Article
- Reversing transgene silencing via targeted chromatin editing.bioRxiv : the preprint server for biology · 2025Article
- H3K4me3 amplifies transcription at intergenic active regulatory elements.Genes & development · 2025Article
- Epigenetic alterations facilitate transcriptional and translational programs in hypoxia.Nature cell biology · 2025Article
- Functional dissection of H3K4 methyltransferases reveals distinct catalytic and non-catalytic roles in C. elegans development.Development (Cambridge, England) · 2025Article
- Human opsin restoration by histone methylation using methyltransferase fusion protein SETD7-dCas9.Molecular therapy. Nucleic acids · 2025Article
- Epithelial Memory After Respiratory Viral Infection in Mice Results in Prolonged Enhancement of Antigen Presentation.Allergy · 2025Article
- Development of compact transcriptional effectors using high-throughput measurements in diverse contexts.Nature biotechnology · 2025Article
- Epigenetic editing and epi-drugs: a combination strategy to simultaneously target KDM4 as a novel anticancer approach.Clinical epigenetics · 2025Article
- CRISPR Epigenome Editing in Human Cells using Plasmid DNA Transfection and mRNA Nucleofection Delivery.Journal of visualized experiments : JoVE · 2025Article
86 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors.
Funding
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Abstract
Histone modifications reflect gene activity, but the relationship between cause and consequence of transcriptional control is heavily debated. Recent developments in rewriting local histone codes of endogenous genes elucidated instructiveness of certain marks in regulating gene expression. Maintenance of such repressive epigenome editing is controversial, while stable reactivation is still largely unexplored. Here we demonstrate sustained gene re-expression using two types of engineered DNA-binding domains fused to a H3K4 methyltransferase. Local induction of H3K4me3 is sufficient to allow re-expression of silenced target genes in various cell types. Maintenance of the re-expression is achieved, but strongly depends on the chromatin microenvironment (that is, DNA methylation status). We further identify H3K79me to be essential in allowing stable gene re-expression, confirming its role in epigenetic crosstalk for stable reactivation. Our approach uncovers potent epigenetic modifications to be directly written onto genomic loci to stably activate any given gene.
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