ArticleProceedings of the National Academy of Sciences of the United States of America2002
Suppression of genome instability by redundant S-phase checkpoint pathways in Saccharomyces cerevisiae.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
What it found
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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
77 citing papers in PubMed, 144 citations in OpenAlex.
- Signification and Application of Mutator and Antimutator Phenotype-Induced Genetic Variations in Evolutionary Adaptation and Cancer Therapeutics.Journal of microbiology (Seoul, Korea) · 2023Review
- Flexible Attachment and Detachment of Centromeres and Telomeres to and from Chromosomes.Biomolecules · 2023Review
- Article
- A rapidly reversible mutation generates subclonal genetic diversity and unstable drug resistance.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Swr1 chromatin-remodeling complex prevents genome instability induced by replication fork progression defects.Nature communications · 2018Article
- Pathways and Mechanisms that Prevent Genome Instability inGenetics · 2017Review
- PARP3 is a promoter of chromosomal rearrangements and limits G4 DNA.Nature communications · 2017Article
- Nucleolytic processing of aberrant replication intermediates by an Exo1-Dna2-Sae2 axis counteracts fork collapse-driven chromosome instability.Nucleic acids research · 2016Article
- hPso4/hPrp19: a critical component of DNA repair and DNA damage checkpoint complexes.Oncogene · 2016Review
- Yet another job for Dna2: Checkpoint activation.DNA repair · 2015Review
- Directed Evolution of RecA Variants with Enhanced Capacity for Conjugational Recombination.PLoS genetics · 2015Article
- The dissolution of double Holliday junctions.Cold Spring Harbor perspectives in biology · 2014Review
- The extent of error-prone replication restart by homologous recombination is controlled by Exo1 and checkpoint proteins.Journal of cell science · 2014Article
- The DNA damage checkpoint pathway promotes extensive resection and nucleotide synthesis to facilitate homologous recombination repair and genome stability in fission yeast.Nucleic acids research · 2014Article
- Article
- Signaling of double strand breaks and deprotected telomeres in Arabidopsis.Frontiers in plant science · 2013Review
- A negative genetic interaction map in isogenic cancer cell lines reveals cancer cell vulnerabilities.Molecular systems biology · 2013Article
- Article
- Lagging strand maturation factor Dna2 is a component of the replication checkpoint initiation machinery.Genes & development · 2013Article
- The DNA damage checkpoint response to replication stress: A Game of Forks.Frontiers in genetics · 2013Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cancer cells show increased genome rearrangements, although it is unclear what defects cause these rearrangements. Previous studies have implicated the Saccharomyces cerevisiae replication checkpoint in the suppression of spontaneous genome rearrangements. In the present study, low doses of methyl methane sulfonate that activate the intra-S checkpoint but not the G1 or G2 DNA damage checkpoints were found to cause increased accumulation of genome rearrangements in both wild-type strains and to an even greater extent in strains containing mutations causing defects in the intra-S checkpoint. The rearrangements were primarily translocations or events resulting in deletion of a portion of a chromosome arm along with the addition of a new telomere. Combinations of mutations causing individual defects in the RAD24 or SGS1 branches of the intra-S checkpoint or the replication checkpoint showed synergistic interactions with regard to the spontaneous genome instability rate. PDS1 and the RAD50-MRE11-XRS2 complex were found to be important members of all the S-phase checkpoints in suppressing genome instability, whereas RAD53 only seemed to play a role in the intra-S checkpoints. Combinations of mutations that seem to result in inactivation of the S-phase checkpoints and critical effectors resulted in as much as 12,000-14,000-fold increases in the genome instability rate. These data support the view that spontaneous genome rearrangements result from DNA replication errors and indicate that there is a high degree of redundancy among the checkpoints that act in S phase to suppress such genome instability.
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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.