ArticleNature communications2021
The RAD51 recombinase protects mitotic chromatin in human cells.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 53 citations in OpenAlex.
- Distinct functions of mammalian RAD51 paralogs in genome maintenance.Biochemical Society transactions · 2026Review
- Mitotic kinase regulation of DNA replication forks.bioRxiv : the preprint server for biology · 2026Article
- TOPBP1-PLK1 interaction preserves genome integrity during mitosis.Nucleic acids research · 2026Article
- Response Factor Correction for Quantitative Determination of HomooligomericJournal of the American Society for Mass Spectrometry · 2026Article
- Cancer-associated USP28 missense mutations disrupt 53BP1 interaction and p53 stabilization.Nature communications · 2025Article
- High-throughput screening identifies a previously undescribed checkpoint controlling mitotic progression in response to DNA damage.The FEBS journal · 2025Article
- RAD51 is chromatin enriched and targetable in BRCA1-deficient cells.Molecular cell · 2025Article
- Review
- DNA double-strand break end resection factors and WRN facilitate mitotic DNA synthesis in human cells.Nature communications · 2025Article
- Ivabradine induces RAD51 degradation, potentiating PARP inhibitor efficacy in non-germline BRCA pathogenic variant triple-negative breast cancer.Journal of translational medicine · 2025Article
- TopBP1 coordinates DNA repair synthesis in mitosis via recruitment of the nuclease scaffold SLX4.Communications biology · 2025Article
- USP28 promotes PARP inhibitor resistance by enhancing SOX9-mediated DNA damage repair in ovarian cancer.Cell death & disease · 2025Article
- CDK1 mediates the metabolic regulation of DNA double-strand break repair in metaphase II oocytes.BMC biology · 2025Article
- Combined inhibition of RAD51 and CHK1 causes synergistic toxicity in cisplatin resistant cancer cells by triggering replication fork collapse.International journal of cancer · 2025Article
- E2F1-mediatedCytoJournal · 2025Article
- In silico structural analysis of Oryza sativa RAD51 reveals key interactions for nucleoprotein filament assembly and regulation.PloS one · 2025Article
- Roles of chromatin and genome instability in cellular senescence and their relevance to ageing and related diseases.Nature reviews. Molecular cell biology · 2024Review
- Polyubiquitinated PCNA triggers SLX4-mediated break-induced replication in alternative lengthening of telomeres (ALT) cancer cells.Nucleic acids research · 2024Article
- Human AAA+ ATPase FIGNL1 suppresses RAD51-mediated ultra-fine bridge formation.Nucleic acids research · 2024Article
- Antitumoral Activity of the Universal Methyl DonorMolecules (Basel, Switzerland) · 2024Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The RAD51 recombinase plays critical roles in safeguarding genome integrity, which is fundamentally important for all living cells. While interphase functions of RAD51 in maintaining genome stability are well-characterised, its role in mitosis remains contentious. In this study, we show that RAD51 protects under-replicated DNA in mitotic human cells and, in this way, promotes mitotic DNA synthesis (MiDAS) and successful chromosome segregation. In cells experiencing mild replication stress, MiDAS was detected irrespective of mitotically generated DNA damage. MiDAS broadly required de novo RAD51 recruitment to single-stranded DNA, which was supported by the phosphorylation of RAD51 by the key mitotic regulator Polo-like kinase 1. Importantly, acute inhibition of MiDAS delayed anaphase onset and induced centromere fragility, suggesting a mechanism that prevents the satisfaction of the spindle assembly checkpoint while chromosomal replication remains incomplete. This study hence identifies an unexpected function of RAD51 in promoting genomic stability in mitosis.
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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.