ArticleMolecular and cellular biology2013
The preference for error-free or error-prone postreplication repair in Saccharomyces cerevisiae exposed to low-dose methyl methanesulfonate is cell cycle dependent.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- The Causes for Genomic Instability and How to Try and Reduce Them Through Rational Design of Synthetic DNA.Methods in molecular biology (Clifton, N.J.) · 2024Article
- The DNA damage response acts as a safeguard against harmful DNA-RNA hybrids of different origins.EMBO reports · 2019Article
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- Regulation of HLTF-mediated PCNA polyubiquitination by RFC and PCNA monoubiquitination levels determines choice of damage tolerance pathway.Nucleic acids research · 2018Article
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- Error-free DNA damage tolerance pathway is facilitated by the Irc5 translocase through cohesin.The EMBO journal · 2018Article
- Mapping DNA damage-dependent genetic interactions in yeast via party mating and barcode fusion genetics.Molecular systems biology · 2018Article
- Spatial separation between replisome- and template-induced replication stress signaling.The EMBO journal · 2018Article
- Editor's Highlight: High-Throughput Functional Genomics Identifies Modulators of TCE Metabolite Genotoxicity and Candidate Susceptibility Genes.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
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- Extremely Rare Polymorphisms in Saccharomyces cerevisiae Allow Inference of the Mutational Spectrum.PLoS genetics · 2017Article
- Mutation at a distance caused by homopolymeric guanine repeats in Saccharomyces cerevisiae.Science advances · 2016Article
- DNA Replication Stress Phosphoproteome Profiles Reveal Novel Functional Phosphorylation Sites on Xrs2 in Saccharomyces cerevisiae.Genetics · 2016Article
- Coordination of DNA damage tolerance mechanisms with cell cycle progression in fission yeast.Cell cycle (Georgetown, Tex.) · 2016Article
- Gene-modified embryonic stem cell test to characterize chemical risks.Environmental science and pollution research international · 2015Article
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- Functions of Fun30 chromatin remodeler in regulating cellular resistance to genotoxic stress.PloS one · 2015Article
- Strand-specific analysis shows protein binding at replication forks and PCNA unloading from lagging strands when forks stall.Molecular cell · 2014Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Cells employ error-free or error-prone postreplication repair (PRR) processes to tolerate DNA damage. Here, we present a genome-wide screen for sensitivity to 0.001% methyl methanesulfonate (MMS). This relatively low dose is of particular interest because wild-type cells exhibit no discernible phenotypes in response to treatment, yet PRR mutants are unique among repair mutants in their exquisite sensitivity to 0.001% MMS; thus, low-dose MMS treatment provides a distinctive opportunity to study postreplication repair processes. We show that upon exposure to low-dose MMS, a PRR-defective rad18Δ mutant stalls into a lengthy G2 arrest associated with the accumulation of single-stranded DNA (ssDNA) gaps. Consistent with previous results following UV-induced damage, reactivation of Rad18, even after prolonged G2 arrest, restores viability and genome integrity. We further show that PRR pathway preference in 0.001% MMS depends on timing and context; cells preferentially employ the error-free pathway in S phase and do not require MEC1-dependent checkpoint activation for survival. However, when PRR is restricted to the G2 phase, cells utilize REV3-dependent translesion synthesis, which requires a MEC1-dependent delay and results in significant hypermutability.
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