ArticleNucleic acids research2014
Redundancy of mammalian Y family DNA polymerases in cellular responses to genomic DNA lesions induced by ultraviolet light.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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
23 citing papers in PubMed, 31 citations in OpenAlex.
- Dual role of proliferating cell nuclear antigen monoubiquitination in facilitating Fanconi anemia-mediated interstrand crosslink repair.PNAS nexus · 2024Article
- The Surprising Diversity of UV-Induced Mutations.Advanced genetics (Hoboken, N.J.) · 2024Article
- Polymerase iota (Pol ι) prevents PrimPol-mediated nascent DNA synthesis and chromosome instability.Science advances · 2023Article
- Leveraging the replication stress response to optimize cancer therapy.Nature reviews. Cancer · 2023Review
- Translesion DNA synthesis-driven mutagenesis in very early embryogenesis of fast cleaving embryos.Nucleic acids research · 2022Article
- Division of labor of Y-family polymerases in translesion-DNA synthesis for distinct types of DNA damage.PloS one · 2021Article
- Article
- DNA polymerase δ proofreads errors made by DNA polymerase ε.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- PRIMPOL-Mediated Adaptive Response Suppresses Replication Fork Reversal in BRCA-Deficient Cells.Molecular cell · 2020Article
- Role of Y-family translesion DNA polymerases in replication stress: Implications for new cancer therapeutic targets.DNA repair · 2019Review
- Cooperation between non-essential DNA polymerases contributes to genome stability in Saccharomyces cerevisiae.DNA repair · 2019Article
- DNA polymerase ι is acetylated in response to SScientific reports · 2019Article
- Impact of DNA lesion repair, replication and formation on the mutational spectra of environmental carcinogens: Aflatoxin BDNA repair · 2018Review
- Translesion DNA polymerases in eukaryotes: what makes them tick?Critical reviews in biochemistry and molecular biology · 2017Review
- Mouse DNA polymerase ι lacking the forty-two amino acids encoded by exon-2 is catalytically inactive in vitro.DNA repair · 2017Article
- Eukaryotic DNA Polymerases in Homologous Recombination.Annual review of genetics · 2016Review
- Translesion synthesis mechanisms depend on the nature of DNA damage in UV-irradiated human cells.Nucleic acids research · 2016Article
- WWOX modulates the ATR-mediated DNA damage checkpoint response.Oncotarget · 2016Article
- Mutagenic Bypass of an Oxidized Abasic Lesion-Induced DNA Interstrand Cross-Link Analogue by Human Translesion Synthesis DNA Polymerases.Biochemistry · 2015Article
- DNA sequence context greatly affects the accuracy of bypass across an ultraviolet light 6-4 photoproduct in mammalian cells.Mutation research · 2015Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Short-wave ultraviolet light induces both mildly helix-distorting cyclobutane pyrimidine dimers (CPDs) and severely distorting (6-4) pyrimidine pyrimidone photoproducts ((6-4)PPs). The only DNA polymerase (Pol) that is known to replicate efficiently across CPDs is Polη, a member of the Y family of translesion synthesis (TLS) DNA polymerases. Phenotypes of Polη deficiency are transient, suggesting redundancy with other DNA damage tolerance pathways. Here we performed a comprehensive analysis of the temporal requirements of Y-family Pols ι and κ as backups for Polη in (i) bypassing genomic CPD and (6-4)PP lesions in vivo, (ii) suppressing DNA damage signaling, (iii) maintaining cell cycle progression and (iv) promoting cell survival, by using mouse embryonic fibroblast lines with single and combined disruptions in these Pols. The contribution of Polι is restricted to TLS at a subset of the photolesions. Polκ plays a dominant role in rescuing stalled replication forks in Polη-deficient mouse embryonic fibroblasts, both at CPDs and (6-4)PPs. This dampens DNA damage signaling and cell cycle arrest, and results in increased survival. The role of relatively error-prone Pols ι and κ as backups for Polη contributes to the understanding of the mutator phenotype of xeroderma pigmentosum variant, a syndrome caused by Polη defects.
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