ArticleGenetics2005
Roles of RAD6 epistasis group members in spontaneous polzeta-dependent translesion synthesis in Saccharomyces cerevisiae.
Article in Genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 59 citations in OpenAlex.
- A transient mutational burst occurs during yeast colony development.Molecular systems biology · 2025Article
- Rad18 mediates specific mutational signatures and shapes the genomic landscape of carcinogen-induced tumorsNAR cancer · 2021Article
- Guidelines for DNA recombination and repair studies: Cellular assays of DNA repair pathways.Microbial cell (Graz, Austria) · 2019Review
- The translesion DNA polymerases Pol ζ and Rev1 are activated independently of PCNA ubiquitination upon UV radiation in mutants of DNA polymerase δ.PLoS genetics · 2017Article
- Functions of Ubiquitin and SUMO in DNA Replication and Replication Stress.Frontiers in genetics · 2016Review
- Eukaryotic DNA polymerase ζ.DNA repair · 2015Review
- The POLD3 subunit of DNA polymerase δ can promote translesion synthesis independently of DNA polymerase ζ.Nucleic acids research · 2015Article
- Shared genetic pathways contribute to the tolerance of endogenous and low-dose exogenous DNA damage in yeast.Genetics · 2014Article
- The role of Dbf4-dependent protein kinase in DNA polymerase ζ-dependent mutagenesis in Saccharomyces cerevisiae.Genetics · 2014Article
- Review
- The mechanism of nucleotide excision repair-mediated UV-induced mutagenesis in nonproliferating cells.Genetics · 2013Article
- In vivo bypass of 8-oxodG.PLoS genetics · 2013Article
- DNA polymerase zeta generates clustered mutations during bypass of endogenous DNA lesions in Saccharomyces cerevisiae.Environmental and molecular mutagenesis · 2012Article
- Formaldehyde-induced mutagenesis in Saccharomyces cerevisiae: molecular properties and the roles of repair and bypass systems.Mutation research · 2012Article
- The dCMP transferase activity of yeast Rev1 is biologically relevant during the bypass of endogenously generated AP sites.DNA repair · 2011Article
- Lesion bypass by S. cerevisiae Pol ζ alone.DNA repair · 2011Article
- Article
- Low-fidelity DNA synthesis by the L979F mutator derivative of Saccharomyces cerevisiae DNA polymerase zeta.Nucleic acids research · 2009Article
- The mismatch repair system promotes DNA polymerase zeta-dependent translesion synthesis in yeast.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Eukaryotic translesion polymerases and their roles and regulation in DNA damage tolerance.Microbiology and molecular biology reviews : MMBR · 2009Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
DNA lesions that arise during normal cellular metabolism can block the progress of replicative DNA polymerases, leading to cell cycle arrest and, in higher eukaryotes, apoptosis. Alternatively, such blocking lesions can be temporarily tolerated using either a recombination- or a translesion synthesis-based bypass mechanism. In Saccharomyces cerevisiae, members of the RAD6 epistasis group are key players in the regulation of lesion bypass by the translesion DNA polymerase Polzeta. In this study, changes in the reversion rate and spectrum of the lys2DeltaA746 -1 frameshift allele have been used to evaluate how the loss of members of the RAD6 epistasis group affects Polzeta-dependent mutagenesis in response to spontaneous damage. Our data are consistent with a model in which Polzeta-dependent mutagenesis relies on the presence of either Rad5 or Rad18, which promote two distinct error-prone pathways that partially overlap with respect to lesion specificity. The smallest subunit of Poldelta, Pol32, is also required for Polzeta-dependent spontaneous mutagenesis, suggesting a cooperative role between Poldelta and Polzeta for the bypass of spontaneous lesions. A third error-free pathway relies on the presence of Mms2, but may not require PCNA.
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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.