ArticleBMC biology2004
Evidence for interplay among yeast replicative DNA polymerases alpha, delta and epsilon from studies of exonuclease and polymerase active site mutations.
Article in BMC biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Recombination and Pol ζ Rescue Defective DNA Replication upon Impaired CMG Helicase-Pol ε Interaction.International journal of molecular sciences · 2020Article
- POLE Mutation Spectra Are Shaped by the Mutant Allele Identity, Its Abundance, and Mismatch Repair Status.Molecular cell · 2020Article
- DNA polymerase δ proofreads errors made by DNA polymerase ε.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Excessive excision of correct nucleotides during DNA synthesis explained by replication hurdles.The EMBO journal · 2020Article
- Identification of aViruses · 2018Article
- Article
- Interactions of theOpen biology · 2017Article
- In vivo evidence for translesion synthesis by the replicative DNA polymerase δ.Nucleic acids research · 2016Article
- Genetic instability in budding and fission yeast-sources and mechanisms.FEMS microbiology reviews · 2015Review
- Replicative DNA polymerase δ but not ε proofreads errors in Cis and in Trans.PLoS genetics · 2015Article
- Geminivirus protein structure and function.Molecular plant pathology · 2013Review
- Emergence of DNA polymerase ε antimutators that escape error-induced extinction in yeast.Genetics · 2013Article
- Modulation of mutagenesis in eukaryotes by DNA replication fork dynamics and quality of nucleotide pools.Environmental and molecular mutagenesis · 2012Review
- DNA replication fidelity in Escherichia coli: a multi-DNA polymerase affair.FEMS microbiology reviews · 2012Review
- Antimutator variants of DNA polymerases.Critical reviews in biochemistry and molecular biology · 2011Review
- Mutator suppression and escape from replication error-induced extinction in yeast.PLoS genetics · 2011Article
- A triad interaction in the fingers subdomain of DNA polymerase beta controls polymerase activity.Journal of the American Chemical Society · 2011Article
- Mismatch repair-independent increase in spontaneous mutagenesis in yeast lacking non-essential subunits of DNA polymerase ε.PLoS genetics · 2010Article
- DNA replication fidelity and cancer.Seminars in cancer biology · 2010Review
- DNA polymerases at the eukaryotic fork-20 years later.Mutation research · 2010Review
Corrections and comments
- Erratum issued
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDNA polymerase epsilon (Pol epsilon) is essential for S-phase replication, DNA damage repair and checkpoint control in yeast. A pol2-Y831A mutation leading to a tyrosine to alanine change in the Pol epsilon active site does not cause growth defects and confers a mutator phenotype that is normally subtle but strong in a mismatch repair-deficient strain. Here we investigate the mechanism responsible for the mutator effect.
resultsPurified four-subunit Y831A Pol epsilon turns over more deoxynucleoside triphosphates to deoxynucleoside monophosphates than does wild-type Pol epsilon, suggesting altered coordination between the polymerase and exonuclease active sites. The pol2-Y831A mutation suppresses the mutator effect of the pol2-4 mutation in the exonuclease active site that abolishes proofreading by Pol epsilon, as measured in haploid strain with the pol2-Y831A,4 double mutation. Analysis of mutation rates in diploid strains reveals that the pol2-Y831A allele is recessive to pol2-4. In addition, the mutation rates of strains with the pol2-4 mutation in combination with active site mutator mutations in Pol delta and Pol alpha suggest that Pol epsilon may proofread certain errors made by Pol alpha and Pol delta during replication in vivo.
conclusionsOur data suggest that Y831A replacement in Pol epsilon reduces replication fidelity and its participation in chromosomal replication, but without eliminating an additional function that is essential for viability. This suggests that other polymerases can substitute for certain functions of polymerase epsilon.
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