ArticleGenetics2006
DNA damage checkpoints are involved in postreplication repair.
Article in Genetics, 2006. 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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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
21 citing papers in PubMed, 44 citations in OpenAlex.
- Elevated MSH2 MSH3 expression interferes with DNA metabolism in vivo.Nucleic acids research · 2023Article
- Involvement of budding yeast Rad5 in translesion DNA synthesis through physical interaction with Rev1.Nucleic acids research · 2016Article
- The amino-terminal tails of histones H2A and H3 coordinate efficient base excision repair, DNA damage signaling and postreplication repair in Saccharomyces cerevisiae.Nucleic acids research · 2015Article
- Comparative studies of tri- and hexavalent chromium cytotoxicity and their effects on oxidative state of Saccharomyces cerevisiae cells.Current microbiology · 2014Article
- Article
- DNA-damage tolerance mediated by PCNA*Ub fusions in human cells is dependent on Rev1 but not Polη.Nucleic acids research · 2013Article
- Review
- The preference for error-free or error-prone postreplication repair in Saccharomyces cerevisiae exposed to low-dose methyl methanesulfonate is cell cycle dependent.Molecular and cellular biology · 2013Article
- Site-specific phosphorylation of the DNA damage response mediator rad9 by cyclin-dependent kinases regulates activation of checkpoint kinase 1.PLoS genetics · 2013Article
- Analysis of the tolerance to DNA alkylating damage in MEC1 and RAD53 checkpoint mutants of Saccharomyces cerevisiae.PloS one · 2013Article
- Article
- Rice UBC13, a candidate housekeeping gene, is required for K63-linked polyubiquitination and tolerance to DNA damage.Rice (New York, N.Y.) · 2012Article
- Article
- Specific Roles of MicroRNAs in Their Interactions with Environmental Factors.Journal of nucleic acids · 2012Article
- Lesion bypass by S. cerevisiae Pol ζ alone.DNA repair · 2011Article
- The Saccharomyces cerevisiae RAD9, RAD17 and RAD24 genes are required for suppression of mutagenic post-replicative repair during chronic DNA damage.DNA repair · 2010Article
- Post-replication repair suppresses duplication-mediated genome instability.PLoS genetics · 2010Article
- Maintaining genome stability at the replication fork.Nature reviews. Molecular cell biology · 2010Review
- Mutation analysis of Rad18 in human cancer cell lines and non small cell lung cancer tissues.Journal of experimental & clinical cancer research : CR · 2009Article
- Novel evidences for a tumor suppressor role of Rev3, the catalytic subunit of Pol zeta.Oncogene · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Saccharomyces cerevisiae MMS2 encodes a ubiquitin-conjugating enzyme variant, belongs to the error-free branch of the RAD6 postreplication repair (PRR) pathway, and is parallel to the REV3-mediated mutagenesis branch. A mutation in genes of either the MMS2 or the REV3 branch does not result in extreme sensitivity to DNA-damaging agents; however, deletion of both subpathways of PRR results in a synergistic phenotype. Nevertheless, the double mutant is not as sensitive to DNA-damaging agents as a rad6 or rad18 mutant defective in the entire PRR pathway, suggesting the presence of an additional subpathway within PRR. A synthetic lethal screen was employed in the presence of a sublethal dose of a DNA-damaging agent to identify novel genes involved in PRR, which resulted in the isolation of RAD9 as a candidate PRR gene. Epistatic analysis showed that rad9 is synergistic to both mms2 and rev3 with respect to killing by methyl methanesulfonate (MMS), and the triple mutant is nearly as sensitive as the rad18 single mutant. In addition, rad9 rad18 is no more sensitive to MMS than the rad18 single mutant, suggesting that rad9 plays a role within the PRR pathway. Moreover, deletion of RAD9 reduces damage-induced mutagenesis and the mms2 spontaneous and induced mutagenesis is partially dependent on the RAD9 gene. We further demonstrated that the observed synergistic interactions apply to any two members between different branches of PRR and G1/S and G2/M checkpoint genes. These results suggest that a damage checkpoint is essential for tolerance mediated by both the error-free and error-prone branches of PRR.
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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.