ArticleDNA repair2013
PCNA trimer instability inhibits translesion synthesis by DNA polymerase η and by DNA polymerase δ.
Article in DNA repair, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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
21 citing papers in PubMed, 32 citations in OpenAlex.
- DNA polymerase kappa is the primary translesion synthesis polymerase for aldehyde ICLs.Nucleic acids research · 2025Article
- Proliferating cell nuclear antigen inhibitors block distinct stages of herpes simplex virus infection.PLoS pathogens · 2023Article
- Article
- The inner side of yeast PCNA contributes to genome stability by mediating interactions with Rad18 and the replicative DNA polymerase δ.Scientific reports · 2022Article
- Sequence context effects of replication of Fapy•dG in three mutational hot spot sequences of the p53 gene in human cells.DNA repair · 2021Article
- Photo-activatable Ub-PCNA probes reveal new structural features of the Saccharomyces cerevisiae Polη/PCNA complex.Nucleic acids research · 2021Article
- Interdomain connecting loop and J loop structures determine cross-species compatibility of PCNA.The Journal of biological chemistry · 2021Article
- The PCNA interaction motifs revisited: thinking outside the PIP-box.Cellular and molecular life sciences : CMLS · 2019Article
- DNA polymerase ζ in DNA replication and repair.Nucleic acids research · 2019Review
- Effective mismatch repair depends on timely control of PCNA retention on DNA by the Elg1 complex.Nucleic acids research · 2019Article
- Article
- Destabilization of the PCNA trimer mediated by its interaction with the NEIL1 DNA glycosylase.Nucleic acids research · 2017Article
- Review
- Analyzing the Catalytic Activities and Interactions of Eukaryotic Translesion Synthesis Polymerases.Methods in enzymology · 2017Article
- Identification of New Mutations at the PCNA Subunit Interface that Block Translesion Synthesis.PloS one · 2016Article
- Characterization of proliferating cell nuclear antigen (PCNA) from pathogenic yeast Candida albicans and its functional analyses in S. cerevisiae.BMC microbiology · 2015Article
- Genetic instability in budding and fission yeast-sources and mechanisms.FEMS microbiology reviews · 2015Review
- Dead-End Elimination with a Polarizable Force Field Repacks PCNA Structures.Biophysical journal · 2015Article
- Article
- Chronology in lesion tolerance gives priority to genetic variability.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Translesion synthesis (TLS), the process by which DNA polymerases replicate through DNA lesions, is the source of most DNA damage-induced mutations. Sometimes TLS is carried out by replicative polymerases that have evolved to synthesize DNA on non-damaged templates. Most of the time, however, TLS is carried out by specialized translesion polymerases that have evolved to synthesize DNA on damaged templates. TLS requires the mono-ubiquitylation of the replication accessory factor proliferating cell nuclear antigen (PCNA). PCNA and ubiquitin-modified PCNA (UbPCNA) stimulate TLS by replicative and translesion polymerases. Two mutant forms of PCNA, one with an E113G substitution and one with a G178S substitution, support normal cell growth but inhibit TLS thereby reducing mutagenesis in yeast. A re-examination of the structures of both mutant PCNA proteins revealed substantial disruptions of the subunit interface that forms the PCNA trimer. Both mutant proteins have reduced trimer stability with the G178S substitution causing a more severe defect. The mutant forms of PCNA and UbPCNA do not stimulate TLS of an abasic site by either replicative Pol δ or translesion Pol η. Normal replication by Pol η was also impacted, but normal replication by Pol δ was much less affected. These findings support a model in which reduced trimer stability causes these mutant PCNA proteins to occasionally undergo conformational changes that compromise their ability to stimulate TLS by both replicative and translesion polymerases.
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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.