ArticleNucleic acids research2012
DNA damage bypass operates in the S and G2 phases of the cell cycle and exhibits differential mutagenicity.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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.
The trial behind it
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
70 citing papers in PubMed, 110 citations in OpenAlex.
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- Polyubiquitinated PCNA triggers SLX4-mediated break-induced replication in alternative lengthening of telomeres (ALT) cancer cells.Nucleic acids research · 2024Article
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- Human translesion DNA polymerases ι and κ mediate tolerance to temozolomide in MGMT-deficient glioblastoma cells.DNA repair · 2024Article
- MRNIP limits ssDNA gaps during replication stress.Nucleic acids research · 2024Article
- PARP2 promotes Break Induced Replication-mediated telomere fragility in response to replication stress.Nature communications · 2024Article
- Role of Translesion DNA Synthesis in the Metabolism of Replication-associated Nascent Strand Gaps.Journal of molecular biology · 2024Review
- Cellular Responses to Widespread DNA Replication Stress.International journal of molecular sciences · 2023Review
- Multiple cancers escape from multiple MAPK pathway inhibitors and use DNA replication stress signaling to tolerate aberrant cell cycles.Science signaling · 2023Article
- Generation and Repair of Postreplication Gaps in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2023Review
- Detection of endogenous translesion DNA synthesis in single mammalian cells.Cell reports methods · 2023Article
- Mitotic DNA synthesis in response to replication stress requires the sequential action of DNA polymerases zeta and delta in human cells.Nature communications · 2023Article
- Review
- Changes in the architecture and abundance of replication intermediates delineate the chronology of DNA damage tolerance pathways at UV-stalled replication forks in human cells.Nucleic acids research · 2022Article
- Studying Single-Stranded DNA Gaps at Replication Intermediates by Electron Microscopy.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Genetic and physical interactions between Polη and Rev1 in response to UV-induced DNA damage in mammalian cells.Scientific reports · 2021Article
- Temporally distinct post-replicative repair mechanisms fill PRIMPOL-dependent ssDNA gaps in human cells.Molecular cell · 2021Article
- Targeting protein-protein interactions in the DNA damage response pathways for cancer chemotherapy.RSC chemical biology · 2021Review
10 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
8 authors at 3 institutions in 4 countries.
Funding
Abstract
Translesion DNA synthesis (TLS) employs low-fidelity DNA polymerases to bypass replication-blocking lesions, and being associated with chromosomal replication was presumed to occur in the S phase of the cell cycle. Using immunostaining with anti-replication protein A antibodies, we show that in UV-irradiated mammalian cells, chromosomal single-stranded gaps formed in S phase during replication persist into the G2 phase of the cell cycle, where their repair is completed depending on DNA polymerase ζ and Rev1. Analysis of TLS using a high-resolution gapped-plasmid assay system in cell populations enriched by centrifugal elutriation for specific cell cycle phases showed that TLS operates both in S and G2. Moreover, the mutagenic specificity of TLS in G2 was different from S, and in some cases overall mutation frequency was higher. These results suggest that TLS repair of single-stranded gaps caused by DNA lesions can lag behind chromosomal replication, is separable from it, and occurs both in the S and G2 phases of the cell cycle. Such a mechanism may function to maintain efficient replication, which can progress despite the presence of DNA lesions, with TLS lagging behind and patching regions of discontinuity.
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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.