ArticleMolecular cell2018
Replication Stress Shapes a Protective Chromatin Environment across Fragile Genomic Regions.
Article in Molecular cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 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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Who cites it
68 citing papers in PubMed, 95 citations in OpenAlex.
- Twisting the End Game: How Telomere Chromatin Modifications Shape Telomere Maintenance.Aging cell · 2026Review
- SLX4IP limits replication stress globally and at ALT telomeres.The EMBO journal · 2026Article
- Systematic and Quantitative Investigation of Newly Synthesized Proteins Reveals Distinct Ion Homeostasis and Mitochondrial Changes between Cuproptosis and Ferroptosis in Human Cells.Analytical chemistry · 2026Article
- ATRX loss couples genome instability at a G-rich repeat to dysregulation of human alpha-globin expression.Nature communications · 2026Article
- Superenhancers shape the landscape and repair dynamics of transcription-associated DNA breaks in cancer.Science advances · 2026Article
- Visualizing DNA repair factor recruitment at sites of transcription in single cells.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2026Article
- Ubiquitination of the histone variant mH2A1.2 prevents toxic RAD18 accumulation at a subset of genomic loci upon replication stress.Molecular cell · 2025Article
- Epigenetic control of topoisomerase 1 activity presents a cancer vulnerability.Nature communications · 2025Article
- Isoform-specific function of NSD3 in DNA replication stress confers resistance to PARP inhibitors in prostate cancer.Molecular cell · 2025Article
- Multifunctional histone variants in genome function.Nature reviews. Genetics · 2025Review
- Extracellular Histones Profiles of Pediatric H3K27-Altered Diffuse Midline Glioma.Molecular diagnosis & therapy · 2025Article
- Review
- Aberrant DNA repair reveals a vulnerability in histone H3.3-mutant brain tumors.Nucleic acids research · 2024Article
- Histone H2A variants play a key role at DNA double-strand breaks during repair pathway choice.Frontiers in epigenetics and epigenomics · 2024Review
- Deficiency of histone variant macroH2A1.1 is associated with sexually dimorphic obesity in mice.Scientific reports · 2023Article
- OTUD5 limits replication fork instability by organizing chromatin remodelers.Nucleic acids research · 2023Article
- Article
- macroH2A2 antagonizes epigenetic programs of stemness in glioblastoma.Nature communications · 2023Article
- Emerging role for R-loop formation in hepatocellular carcinoma.Genes & genomics · 2023Review
- Histone H2A variants: Diversifying chromatin to ensure genome integrity.Seminars in cell & developmental biology · 2023Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Recent integrative epigenome analyses highlight the importance of functionally distinct chromatin states for accurate cell function. How these states are established and maintained is a matter of intense investigation. Here, we present evidence for DNA damage as an unexpected means to shape a protective chromatin environment at regions of recurrent replication stress (RS). Upon aberrant fork stalling, DNA damage signaling and concomitant H2AX phosphorylation coordinate the FACT-dependent deposition of macroH2A1.2, a histone variant that promotes DNA repair by homologous recombination (HR). MacroH2A1.2, in turn, facilitates the accumulation of the tumor suppressor and HR effector BRCA1 at replication forks to protect from RS-induced DNA damage. Consequently, replicating primary cells steadily accrue macroH2A1.2 at fragile regions, whereas macroH2A1.2 loss in these cells triggers DNA damage signaling-dependent senescence, a hallmark of RS. Altogether, our findings demonstrate that recurrent DNA damage contributes to the chromatin landscape to ensure the epigenomic integrity of dividing cells.
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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.