ArticlePLoS genetics2015
Replicative DNA polymerase δ but not ε proofreads errors in Cis and in Trans.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 49 citations in OpenAlex.
- Two distinct Okazaki fragment failure modes dominate mutagenesis in the absence of flap endonuclease 1.Nature communications · 2026Article
- Coordinated transfer of DNA between Pol θ and Pol δ resets microhomology choice during double-strand break repair.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Evidence that DNA polymerase δ proofreads errors made by DNA polymerase α across the Saccharomyces cerevisiae nuclear genome.DNA repair · 2024Article
- Base Excision Repair: Mechanisms and Impact in Biology, Disease, and Medicine.International journal of molecular sciences · 2023Review
- Recent Advances in Directed Yeast Genome Evolution.Journal of fungi (Basel, Switzerland) · 2022Review
- Post-Translational Modifications of PCNA: Guiding for the Best DNA Damage Tolerance Choice.Journal of fungi (Basel, Switzerland) · 2022Review
- How asymmetric DNA replication achieves symmetrical fidelity.Nature structural & molecular biology · 2021Article
- Expression of the cancer-associated DNA polymerase ε P286R in fission yeast leads to translesion synthesis polymerase dependent hypermutation and defective DNA replication.PLoS genetics · 2021Article
- Mutagenic mechanisms of cancer-associated DNA polymerase ϵ alleles.Nucleic acids research · 2021Article
- Mechanisms for Maintaining Eukaryotic Replisome Progression in the Presence of DNA Damage.Frontiers in molecular biosciences · 2021Review
- DNA Polymerases at the Eukaryotic Replication Fork Thirty Years after: Connection to Cancer.Cancers · 2020Review
- Article
- Opportunities for new studies of nuclear DNA replication enzymology in budding yeast.Current genetics · 2020Review
- DNA polymerase δ proofreads errors made by DNA polymerase ε.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Molecular and structural characterization of oxidized ribonucleotide insertion into DNA by human DNA polymerase β.The Journal of biological chemistry · 2020Article
- Article
- The absence of the catalytic domains of Saccharomyces cerevisiae DNA polymerase ϵ strongly reduces DNA replication fidelity.Nucleic acids research · 2019Article
- Insights into DNA polymerase δ's mechanism for accurate DNA replication.Journal of molecular modeling · 2019Article
- Structural consequence of the most frequently recurring cancer-associated substitution in DNA polymerase ε.Nature communications · 2019Article
- A recurrent cancer-associated substitution in DNA polymerase ε produces a hyperactive enzyme.Nature communications · 2019Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
It is now well established that in yeast, and likely most eukaryotic organisms, initial DNA replication of the leading strand is by DNA polymerase ε and of the lagging strand by DNA polymerase δ. However, the role of Pol δ in replication of the leading strand is uncertain. In this work, we use a reporter system in Saccharomyces cerevisiae to measure mutation rates at specific base pairs in order to determine the effect of heterozygous or homozygous proofreading-defective mutants of either Pol ε or Pol δ in diploid strains. We find that wild-type Pol ε molecules cannot proofread errors created by proofreading-defective Pol ε molecules, whereas Pol δ can not only proofread errors created by proofreading-defective Pol δ molecules, but can also proofread errors created by Pol ε-defective molecules. These results suggest that any interruption in DNA synthesis on the leading strand is likely to result in completion by Pol δ and also explain the higher mutation rates observed in Pol δ-proofreading mutants compared to Pol ε-proofreading defective mutants. For strains reverting via AT→GC, TA→GC, CG→AT, and GC→AT mutations, we find in addition a strong effect of gene orientation on mutation rate in proofreading-defective strains and demonstrate that much of this orientation dependence is due to differential efficiencies of mispair elongation. We also find that a 3'-terminal 8 oxoG, unlike a 3'-terminal G, is efficiently extended opposite an A and is not subject to proofreading. Proofreading mutations have been shown to result in tumor formation in both mice and humans; the results presented here can help explain the properties exhibited by those proofreading mutants.
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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.