ArticleNucleic acids research2014
The DNA damage checkpoint pathway promotes extensive resection and nucleotide synthesis to facilitate homologous recombination repair and genome stability in fission yeast.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 31 citations in OpenAlex.
- Keep calm and reboot - how cells restart transcription after DNA damage and DNA repair.FEBS letters · 2025Review
- Identification of RAD17 as a candidate cancer predisposition gene in families with histories of pancreatic and breast cancers.BMC cancer · 2024Article
- Gross Chromosomal Rearrangement at Centromeres.Biomolecules · 2023Review
- Flexible Attachment and Detachment of Centromeres and Telomeres to and from Chromosomes.Biomolecules · 2023Review
- Fission yeast Srr1 and Skb1 promote isochromosome formation at the centromere.Communications biology · 2023Article
- Homologous recombination suppresses transgenerational DNA end resection and chromosomal instability in fission yeast.Nucleic acids research · 2023Article
- Multiple 9-1-1 complexes promote homolog synapsis, DSB repair, and ATR signaling during mammalian meiosis.eLife · 2022Article
- MRN-dependent and independent pathways for recruitment of TOPBP1 to DNA double-strand breaks.PloS one · 2022Article
- Fission yeast Rad8/HLTF facilitates Rad52-dependent chromosomal rearrangements through PCNA lysine 107 ubiquitination.PLoS genetics · 2021Article
- An essential role for dNTP homeostasis following CDK-induced replication stress.Journal of cell science · 2019Article
- Guidelines for DNA recombination and repair studies: Cellular assays of DNA repair pathways.Microbial cell (Graz, Austria) · 2019Review
- OsRAD17 Is Required for Meiotic Double-Strand Break Repair and Plays a Redundant Role With OsZIP4 in Synaptonemal Complex Assembly.Frontiers in plant science · 2018Article
- Rgf1p (Rho1p GEF) is required for double-strand break repair in fission yeast.Nucleic acids research · 2017Article
- The Exonuclease Homolog OsRAD1 Promotes Accurate Meiotic Double-Strand Break Repair by Suppressing Nonhomologous End Joining.Plant physiology · 2016Article
- Predicting chemotherapeutic drug combinations through gene network profiling.Scientific reports · 2016Article
- The checkpoint clamp protein Rad9 facilitates DNA-end resection and prevents alternative non-homologous end joining.Cell cycle (Georgetown, Tex.) · 2014Article
- The 9-1-1 checkpoint clamp stimulates DNA resection by Dna2-Sgs1 and Exo1.Nucleic acids research · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
DNA double-strand breaks (DSBs) can cause chromosomal rearrangements and extensive loss of heterozygosity (LOH), hallmarks of cancer cells. Yet, how such events are normally suppressed is unclear. Here we identify roles for the DNA damage checkpoint pathway in facilitating homologous recombination (HR) repair and suppressing extensive LOH and chromosomal rearrangements in response to a DSB. Accordingly, deletion of Rad3(ATR), Rad26ATRIP, Crb2(53BP1) or Cdc25 overexpression leads to reduced HR and increased break-induced chromosome loss and rearrangements. We find the DNA damage checkpoint pathway facilitates HR, in part, by promoting break-induced Cdt2-dependent nucleotide synthesis. We also identify additional roles for Rad17, the 9-1-1 complex and Chk1 activation in facilitating break-induced extensive resection and chromosome loss, thereby suppressing extensive LOH. Loss of Rad17 or the 9-1-1 complex results in a striking increase in break-induced isochromosome formation and very low levels of chromosome loss, suggesting the 9-1-1 complex acts as a nuclease processivity factor to facilitate extensive resection. Further, our data suggest redundant roles for Rad3ATR and Exo1 in facilitating extensive resection. We propose that the DNA damage checkpoint pathway coordinates resection and nucleotide synthesis, thereby promoting efficient HR repair and genome stability.
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.