ArticlePLoS genetics2013
Genome-wide screen reveals replication pathway for quasi-palindrome fragility dependent on homologous recombination.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
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.
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Who cites it
28 citing papers in PubMed, 35 citations in OpenAlex.
- Genome-wide screen reveals dependence of break induced replication on several distinct checkpoints.Nature communications · 2025Article
- Overcoming natural replication barriers formed by DNA structures and the role of repositioning to the nuclear periphery.DNA repair · 2025Review
- Identification of different classes of genome instability suppressor genes through analysis of DNA damage response markers.G3 (Bethesda, Md.) · 2024Article
- Massive contractions of myotonic dystrophy type 2-associated CCTG tetranucleotide repeats occur via double-strand break repair with distinct requirements for DNA helicases.G3 (Bethesda, Md.) · 2024Article
- Widely spaced and divergent inverted repeats become a potent source of chromosomal rearrangements in long single-stranded DNA regions.Nucleic acids research · 2023Article
- Partners in crime: Tbf1 and Vid22 promote expansions of long human telomeric repeats at an interstitial chromosome position in yeast.PNAS nexus · 2022Article
- Computational detection of a genome instability-derived lncRNA signature for predicting the clinical outcome of lung adenocarcinoma.Cancer medicine · 2022Article
- Characterization of canavanine-resistance of cat1 and vhc1 deletions and a dominant any1 mutation in fission yeast.PloS one · 2022Article
- Structural parameters of palindromic repeats determine the specificity of nuclease attack of secondary structures.Nucleic acids research · 2021Article
- Palindromes in DNA-A Risk for Genome Stability and Implications in Cancer.International journal of molecular sciences · 2021Review
- Alternative DNA StructuresMicrobiology and molecular biology reviews : MMBR · 2021Review
- Genetic and Molecular Approaches to Study Chromosomal Breakage at Secondary Structure-Forming Repeats.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Replication stress at microsatellites causes DNA double-strand breaks and break-induced replication.The Journal of biological chemistry · 2020Article
- Mechanisms underlying genome instability mediated by formation of foldback inversions ineLife · 2020Article
- Topoisomerase II contributes to DNA secondary structure-mediated double-stranded breaks.Nucleic acids research · 2020Article
- Genetic Screens to Study GAA/TTC and Inverted Repeat Instability in Saccharomyces cerevisiae.Methods in molecular biology (Clifton, N.J.) · 2020Article
- Generic Repeat Finder: A High-Sensitivity Tool for Genome-Wide De Novo Repeat Detection.Plant physiology · 2019Article
- Genome-wide analysis of genomic alterations induced by oxidative DNA damage in yeast.Nucleic acids research · 2019Article
- Genome-wide Identification of Structure-Forming Repeats as Principal Sites of Fork Collapse upon ATR Inhibition.Molecular cell · 2018Article
- Cis- and Trans-Modifiers of Repeat Expansions: Blending Model Systems with Human Genetics.Trends in genetics : TIG · 2018Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Inverted repeats capable of forming hairpin and cruciform structures present a threat to chromosomal integrity. They induce double strand breaks, which lead to gross chromosomal rearrangements, the hallmarks of cancers and hereditary diseases. Secondary structure formation at this motif has been proposed to be the driving force for the instability, albeit the mechanisms leading to the fragility are not well-understood. We carried out a genome-wide screen to uncover the genetic players that govern fragility of homologous and homeologous Alu quasi-palindromes in the yeast Saccharomyces cerevisiae. We found that depletion or lack of components of the DNA replication machinery, proteins involved in Fe-S cluster biogenesis, the replication-pausing checkpoint pathway, the telomere maintenance complex or the Sgs1-Top3-Rmi1 dissolvasome augment fragility at Alu-IRs. Rad51, a component of the homologous recombination pathway, was found to be required for replication arrest and breakage at the repeats specifically in replication-deficient strains. These data demonstrate that Rad51 is required for the formation of breakage-prone secondary structures in situations when replication is compromised while another mechanism operates in DSB formation in replication-proficient strains.
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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.