ArticleNature communications2025
H3K36 Methylation as a Guardian of Epigenome Integrity.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Single-cell and spatial transcriptomics reveal SUV39H1 as a master epigenetic driver of immunosuppressive niche and stemness in bladder cancer.Translational oncology · 2026Article
- Histone tail mutants: versatile tools for decoding chromatin, development, and disease.Trends in genetics : TIG · 2026Review
- Single cell CRISPR screen identifies antagonism between Nsd1-H3K36me2 and Ezh2-H3K27me3 orchestrates pluripotency transition.Stem cell reports · 2026Article
- Long-term maintenance of H3K27me3 in postmitotic neurons is dispensable for gene expression regulation.bioRxiv : the preprint server for biology · 2026Article
- DNMT1 loss leads to hypermethylation of a subset of late replicating domains by DNMT3A.PLoS genetics · 2026Article
- H3K36 Methylation as a Guardian of Epigenome Integrity.Nature communications · 2025Article
- ChIPbinner: an R package for analyzing broad histone marks binned in uniform windows from ChIP-Seq or CUT&RUN/TAG data.BMC bioinformatics · 2025Article
- The Histone Methyltransferase OsSET37 Positively Regulates Rice Seed Vigor.Physiologia plantarumArticle
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
H3K36 methylation is a key epigenetic mark with critical roles in development and disease. Here, we systematically dissect its functions using CRISPR-engineered mouse mesenchymal stem cells lacking combinations of the five H3K36 methyltransferases, culminating in quintuple knockout cells devoid of H3K36me2/3. We show that H3K36me2 influences enhancer activity, supports the expression of their target genes, and safeguards active genes from encroachment of the repressive marks, H3K27me2/3. In addition, we find that the loss of H3K36me triggers redistribution of large heterochromatic H3K9me3 domains into euchromatin, in part mediated by SUV39H1, leading to global epigenomic remodelling, constitutive heterochromatin erosion, and a collapse of 3D genome organization. Parallel analyses in human HNSCC cells overexpressing the H3K36M oncohistone reveal conserved disruptions to the epigenome and chromatin architecture. Together, these results establish H3K36 methylation as a pivotal regulator of chromatin state and genomic structure.
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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.