ArticleNature communications2023
Mitotic DNA synthesis in response to replication stress requires the sequential action of DNA polymerases zeta and delta in human cells.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 46 citations in OpenAlex.
- HELQ & Hel308: ancient enzymes of DNA repair and recombination.Biochemical Society transactions · 2026Review
- DDX3X regulates DNA repair pathway choice at double-strand breaks via RNA-DNA hybrid formation.Cell death and differentiation · 2026Article
- Vitamin D3 ameliorates R-loop-induced replication stress and chromosomal instability in MED12-mutant uterine fibroids.Scientific reports · 2026Article
- CIP2A recruits SLX4-MUS81-XPF in mitosis and protects against replication stress.EMBO reports · 2026Article
- Mitotic kinase regulation of DNA replication forks.bioRxiv : the preprint server for biology · 2026Article
- Mitotic microhomology-mediated break-induced replication promotes chromoanasynthesis.Nature communications · 2026Article
- Vitamin D3 ameliorates R-loop-induced replication stress and chromosomal instability in MED12-mutant uterine fibroids.Research square · 2026Article
- Mitotic DNA repair by TMEJ suppresses replication stress-induced nuclear envelope reassembly defect.Nature communications · 2025Article
- DNA double-strand break end resection factors and WRN facilitate mitotic DNA synthesis in human cells.Nature communications · 2025Article
- Review
- DNA polymerase zeta can efficiently replicate structures formed by AT/TA repeat sequences and prevent their deletion.Nucleic acids research · 2025Article
- Old Passengers as New Drivers: Chromosomal Passenger Proteins Engage in Translesion Synthesis.Cells · 2024Article
- Polyubiquitinated PCNA triggers SLX4-mediated break-induced replication in alternative lengthening of telomeres (ALT) cancer cells.Nucleic acids research · 2024Article
- USP9X-mediated REV1 deubiquitination promotes lung cancer radioresistance via the action of REV1 as a Rad18 molecular scaffold for cystathionine γ-lyase.Journal of biomedical science · 2024Article
- Transient ZnProceedings of the National Academy of Sciences of the United States of America · 2024Article
- A perspective on tumor radiation resistance following high-LET radiation treatment.Journal of cancer research and clinical oncology · 2024Review
- PARP2 promotes Break Induced Replication-mediated telomere fragility in response to replication stress.Nature communications · 2024Article
- Review
- FANCD2-dependent mitotic DNA synthesis relies on PCNA K164 ubiquitination.Cell reports · 2023Article
- REV7 Monomer Is Unable to Participate in Double Strand Break Repair and Translesion Synthesis but Suppresses Mitotic Errors.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncogene activation creates DNA replication stress (RS) in cancer cells, which can generate under-replicated DNA regions (UDRs) that persist until cells enter mitosis. UDRs also have the potential to generate DNA bridges in anaphase cells or micronuclei in the daughter cells, which could promote genomic instability. To suppress such damaging changes to the genome, human cells have developed a strategy to conduct 'unscheduled' DNA synthesis in mitosis (termed MiDAS) that serves to rescue under-replicated loci. Previous studies have shown that MiDAS proceeds via a POLD3-dependent pathway that shows some features of break-induced replication. Here, we define how human cells utilize both DNA gap filling (REV1 and Pol ζ) and replicative (Pol δ) DNA polymerases to complete genome duplication following a perturbed S-phase. We present evidence for the existence of a polymerase-switch during MiDAS that is required for new DNA synthesis at UDRs. Moreover, we reveal that, upon oncogene activation, cancer cell survival is significantly compromised when REV1 is depleted, suggesting that REV1 inhibition might be a feasible approach for the treatment of some human cancers.
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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.