ArticleNature communications2020
H3K4 methylation at active genes mitigates transcription-replication conflicts during replication stress.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 61 citations in OpenAlex.
- A systematic interactome ofeLife · 2026Article
- Rpd3L regulates transcription-replication conflict via H3K4 methylation-dependent and -independent chromatin mechanisms.Science advances · 2026Article
- Induced DNA double strand breaks by genotoxic drugs occur at active transcription H3K36 tri-methylation sites.Communications biology · 2026Article
- WDR-5 exhibits H3K4 methylation-independent activity during embryonic development in C. elegans.Epigenetics & chromatin · 2026Article
- Chromatin state dynamics during the Plasmodium falciparum intraerythrocytic development cycle.BMC genomics · 2026Article
- Epigenetic regulation by DNA methylation, histone modifications and chromatin remodeling complexes in controlling spermatogenesis and their dysfunction with male infertility.Cellular and molecular life sciences : CMLS · 2025Review
- Epigenetic regulation of intracellular branched-chain amino acid homeostasis maintains a normal lifespan.iScience · 2025Article
- ZC3H4 safeguards genome integrity by preventing transcription-replication conflicts at noncoding RNA loci.Science advances · 2025Article
- NSUN2-mediated HCV RNA m5C Methylation Facilitates Viral RNA Stability and Replication.Genomics, proteomics & bioinformatics · 2025Article
- Wdr5-mediated H3K4 methylation facilitates HSPC development via maintenance of genomic stability in zebrafish.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Transcription-replication conflicts drive R-loop-dependent nucleosome eviction and require DOT1L activity for transcription recovery.Nucleic acids research · 2025Article
- HPathogens (Basel, Switzerland) · 2024Review
- Developmental signals control chromosome segregation fidelity during pluripotency and neurogenesis by modulating replicative stress.Nature communications · 2024Article
- The Rtf1/Prf1-dependent histone modification axis counteracts multi-drug resistance in fission yeast.Life science alliance · 2024Article
- Adult Human, but Not Rodent, Spermatogonial Stem Cells Retain States with a Foetal-like Signature.Cells · 2024Article
- Review
- Increased H3K9me3 and F-Actin Reorganization in the Rapid Adaptive Response to Hypergravity in Human T Lymphocytes.International journal of molecular sciences · 2023Article
- Transcription-Replication Conflicts as a Source of Genome Instability.Annual review of genetics · 2023Review
- The COMPASS subunit Spp1 protects nascent DNA at the Tus/Ter replication fork barrier by limiting DNA availability to nucleases.Nature communications · 2023Article
- Diverse and dynamic forms of gene regulation by the S. cerevisiae histone methyltransferase Set1.Current genetics · 2023Review
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
Abstract
Transcription-replication conflicts (TRCs) occur when intensive transcriptional activity compromises replication fork stability, potentially leading to gene mutations. Transcription-deposited H3K4 methylation (H3K4me) is associated with regions that are susceptible to TRCs; however, the interplay between H3K4me and TRCs is unknown. Here we show that H3K4me aggravates TRC-induced replication failure in checkpoint-defective cells, and the presence of methylated H3K4 slows down ongoing replication. Both S-phase checkpoint activity and H3K4me are crucial for faithful DNA synthesis under replication stress, especially in highly transcribed regions where the presence of H3K4me is highest and TRCs most often occur. H3K4me mitigates TRCs by decelerating ongoing replication, analogous to how speed bumps slow down cars. These findings establish the concept that H3K4me defines the transcriptional status of a genomic region and defends the genome from TRC-mediated replication stress and instability.
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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.