ArticleMolecular cell2023
SLFN5-mediated chromatin dynamics sculpt higher-order DNA repair topology.
Article in Molecular cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Folding a broken genome: the versatile roles of cohesin in genome maintenance.Nature reviews. Genetics · 2026Review
- SLFN5 restrains type I interferon responses and promotes glioblastoma via its N-terminal Schlafen core domain.Communications biology · 2026Article
- Methodological Landscape of DNA Damage Response Detection: From Conventional Assays to Future Innovations.Current issues in molecular biology · 2026Review
- Schlafen 5 is an intracellular immune checkpoint and controls IFN responses in pancreatic ductal adenocarcinoma.JCI insight · 2026Article
- Improving PARP inhibitor efficacy in bladder cancer without genetic BRCAness by combination with PLX51107.Molecular oncology · 2026Article
- Article
- Nuclear and genome dynamics underlying DNA double-strand break repair.Nature reviews. Molecular cell biology · 2025Review
- CREPT is required for the metastasis of triple-negative breast cancer through a co-operational-chromatin loop-based gene regulation.Molecular cancer · 2025Article
- Genome-wide profiling of DNA repair proteins in single cells.Nature communications · 2024Article
- Cell-specific cross-talk proteomics reveals cathepsin B signaling as a driver of glioblastoma malignancy near the subventricular zone.Science advances · 2024Article
- Mouse Slfn8 and Slfn9 genes complement human cells lacking SLFN11 during the replication stress response.Communications biology · 2023Article
- Progress in investigating the relationship between Schlafen5 genes and malignant tumors.Frontiers in oncology · 2023Review
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Authors and funding
23 authors at 5 institutions in 2 countries.
Funding
Abstract
Repair of DNA double-strand breaks (DSBs) elicits three-dimensional (3D) chromatin topological changes. A recent finding reveals that 53BP1 assembles into a 3D chromatin topology pattern around DSBs. How this formation of a higher-order structure is configured and regulated remains enigmatic. Here, we report that SLFN5 is a critical factor for 53BP1 topological arrangement at DSBs. Using super-resolution imaging, we find that SLFN5 binds to 53BP1 chromatin domains to assemble a higher-order microdomain architecture by driving damaged chromatin dynamics at both DSBs and deprotected telomeres. Mechanistically, we propose that 53BP1 topology is shaped by two processes: (1) chromatin mobility driven by the SLFN5-LINC-microtubule axis and (2) the assembly of 53BP1 oligomers mediated by SLFN5. In mammals, SLFN5 deficiency disrupts the DSB repair topology and impairs non-homologous end joining, telomere fusions, class switch recombination, and sensitivity to poly (ADP-ribose) polymerase inhibitor. We establish a molecular mechanism that shapes higher-order chromatin topologies to safeguard genomic stability.
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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.