ArticleMolecular and cellular biology2005
Saccharomyces cerevisiae as a model system to define the chromosomal instability phenotype.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed.
- Stabilization of expandable DNA repeats by the replication factor Mcm10 promotes cell viability.Nature communications · 2024Article
- A mapping platform for mitotic crossover by single-cell multi-omics.Methods in enzymology · 2021Article
- EssentialProceedings of the National Academy of Sciences of the United States of America · 2019Article
- The Swr1 chromatin-remodeling complex prevents genome instability induced by replication fork progression defects.Nature communications · 2018Article
- SUMO E3 ligase Mms21 prevents spontaneous DNA damage induced genome rearrangements.PLoS genetics · 2018Article
- Regulation of mitotic recombination between DNA repeats in centromeres.Nucleic acids research · 2017Article
- Pathways and Mechanisms that Prevent Genome Instability inGenetics · 2017Review
- A genetic network that suppresses genome rearrangements in Saccharomyces cerevisiae and contains defects in cancers.Nature communications · 2016Article
- Mre11-Sae2 and RPA Collaborate to Prevent Palindromic Gene Amplification.Molecular cell · 2015Article
- The Ty1 LTR-retrotransposon of budding yeast,Microbiology spectrum · 2015Article
- Yeast Assay Highlights the Intrinsic Genomic Instability of Human PML Intron 6 over Intron 3 and the Role of Replication Fork Proteins.PloS one · 2015Article
- Review
- DNA repair pathway selection caused by defects in TEL1, SAE2, and de novo telomere addition generates specific chromosomal rearrangement signatures.PLoS genetics · 2014Article
- Mapping genomic hotspots of DNA damage by a single-strand-DNA-compatible and strand-specific ChIP-seq method.Genome research · 2013Article
- Recurrent rearrangement during adaptive evolution in an interspecific yeast hybrid suggests a model for rapid introgression.PLoS genetics · 2013Article
- Gene copy-number variation in haploid and diploid strains of the yeast Saccharomyces cerevisiae.Genetics · 2013Article
- Bioinformatic identification of genes suppressing genome instability.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Microhomology directs diverse DNA break repair pathways and chromosomal translocations.PLoS genetics · 2012Article
- Differential genetic interactions between Sgs1, DNA-damage checkpoint components and DNA repair factors in the maintenance of chromosome stability.Genome integrity · 2011Article
- AID induces double-strand breaks at immunoglobulin switch regions and c-MYC causing chromosomal translocations in yeast THO mutants.PLoS genetics · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Translocations, deletions, and chromosome fusions are frequent events seen in cancers with genome instability. Here we analyzed 358 genome rearrangements generated in Saccharomyces cerevisiae selected by the loss of the nonessential terminal segment of chromosome V. The rearrangements appeared to be generated by both nonhomologous end joining and homologous recombination and targeted all chromosomes. Fifteen percent of the rearrangements occurred independently more than once. High levels of specific classes of rearrangements were isolated from strains with specific mutations: translocations to Ty elements were increased in telomerase-defective mutants, potential dicentric translocations and dicentric isochromosomes were associated with cell cycle checkpoint defects, chromosome fusions were frequent in strains with both telomerase and cell cycle checkpoint defects, and translocations to homolog genes were seen in strains with defects allowing homoeologous recombination. An analysis of human cancer-associated rearrangements revealed parallels to the effects that strain genotypes have on classes of rearrangement in S. cerevisiae.
Indexed as
Identifiers
What OpenQuestion holds
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.