ArticleMolecular and cellular biology1998
The Saccharomyces cerevisiae RAD9 checkpoint reduces the DNA damage-associated stimulation of directed translocations.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 79 citations in OpenAlex.
- TPI and GAPDH Interact with Rad9, Linking Glycolytic Enzymes to Cancer.International journal of molecular sciences · 2026Article
- Iron, manganese, and copper complexes protect saccharomyces cerevisiae from methyl methanesulfonate-induced genotoxicity and oxidative stress.World journal of microbiology & biotechnology · 2025Article
- Checkpoint and recombination pathways independently suppress rates of spontaneous homology-directed chromosomal translocations in budding yeast.Frontiers in genetics · 2025Article
- Physical interactions between specifically regulated subpopulations of the MCM and RNR complexes prevent genetic instability.PLoS genetics · 2024Article
- An Integrated Approach Reveals DNA Damage and Proteotoxic Stress as Main Effects of Proton Radiation inInternational journal of molecular sciences · 2022Article
- Phosphoproteomics reveals a distinctive Mec1/ATR signaling response upon DNA end hyper-resection.The EMBO journal · 2021Article
- Rad9/53BP1 promotes DNA repair via crossover recombination by limiting the Sgs1 and Mph1 helicases.Nature communications · 2020Article
- Distinct associations of the Saccharomyces cerevisiae Rad9 protein link Mac1-regulated transcription to DNA repair.Current genetics · 2020Article
- CYP1A1 I462V polymorphism is associated with reduced genotoxicity in yeast despite positive association with increased cancer risk.Mutation research. Genetic toxicology and environmental mutagenesis · 2017Article
- BothAIMS genetics · 2017Article
- Activation of aflatoxin B1 by expression of human CYP1A2 polymorphisms in Saccharomyces cerevisiae.Mutation research. Genetic toxicology and environmental mutagenesis · 2014Article
- A Rad53 independent function of Rad9 becomes crucial for genome maintenance in the absence of the Recq helicase Sgs1.PloS one · 2013Article
- Rad59 regulates association of Rad52 with DNA double-strand breaks.MicrobiologyOpen · 2012Article
- The DNA damage checkpoint allows recombination between divergent DNA sequences in budding yeast.DNA repair · 2011Article
- Elevated dNTP levels suppress hyper-recombination in Saccharomyces cerevisiae S-phase checkpoint mutants.Nucleic acids research · 2010Article
- RAD59 and RAD1 cooperate in translocation formation by single-strand annealing in Saccharomyces cerevisiae.Current genetics · 2010Article
- Msh2 blocks an alternative mechanism for non-homologous tail removal during single-strand annealing in Saccharomyces cerevisiae.PloS one · 2009Article
- Faithful after break-up: suppression of chromosomal translocations.Cellular and molecular life sciences : CMLS · 2009Review
- Chromosomal translocations caused by either pol32-dependent or pol32-independent triparental break-induced replication.Molecular and cellular biology · 2009Article
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4 authors at 2 institutions in 1 country.
Funding
Abstract
Genetic instability in the Saccharomyces cerevisiae rad9 mutant correlates with failure to arrest the cell cycle in response to DNA damage. We quantitated the DNA damage-associated stimulation of directed translocations in RAD9+ and rad9 mutants. Directed translocations were generated by selecting for His+ prototrophs that result from homologous, mitotic recombination between two truncated his3 genes, GAL1::his3-delta5' and trp1::his3-delta3'::HOcs. Compared to RAD9+ strains, the rad9 mutant exhibits a 5-fold higher rate of spontaneous, mitotic recombination and a greater than 10-fold increase in the number of UV- and X-ray-stimulated His+ recombinants that contain translocations. The higher level of recombination in rad9 mutants correlated with the appearance of nonreciprocal translocations and additional karyotypic changes, indicating that genomic instability also occurred among non-his3 sequences. Both enhanced spontaneous recombination and DNA damage-associated recombination are dependent on RAD1, a gene involved in DNA excision repair. The hyperrecombinational phenotype of the rad9 mutant was correlated with a deficiency in cell cycle arrest at the G2-M checkpoint by demonstrating that if rad9 mutants were arrested in G2 before irradiation, the numbers both of UV- and gamma-ray-stimulated recombinants were reduced. The importance of G2 arrest in DNA damage-induced sister chromatid exchange (SCE) was evident by a 10-fold reduction in HO endonuclease-induced SCE and no detectable X-ray stimulation of SCE in a rad9 mutant. We suggest that one mechanism by which the RAD9-mediated G2-M checkpoint may reduce the frequency of DNA damage-induced translocations is by channeling the repair of double-strand breaks into SCE.
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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.