ArticleDNA repair2009
Inhibition of DNA double-strand break repair by the Ku heterodimer in mrx mutants of Saccharomyces cerevisiae.
Article in DNA repair, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 40 citations in OpenAlex.
- Article
- Suppression of telomere capping defects of Saccharomyces cerevisiae yku70 and yku80 mutants by telomerase.G3 (Bethesda, Md.) · 2021Article
- Reconsidering pathway choice: a sequential model of mammalian DNA double-strand break pathway decisions.Current opinion in genetics & development · 2021Review
- Loss of vacuolar acidity results in iron-sulfur cluster defects and divergent homeostatic responses during aging in Saccharomyces cerevisiae.GeroScience · 2020Article
- Nej1 Interacts with Mre11 to Regulate Tethering and Dna2 Binding at DNA Double-Strand Breaks.Cell reports · 2019Article
- Genetic Separation of Sae2 Nuclease Activity from Mre11 Nuclease Functions in Budding Yeast.Molecular and cellular biology · 2017Article
- The non-homologous end-joining factor Nej1 inhibits resection mediated by Dna2-Sgs1 nuclease-helicase at DNA double strand breaks.The Journal of biological chemistry · 2017Article
- Consider the workhorse: Nonhomologous end-joining in budding yeast.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2016Review
- Interplay between Ku and Replication Protein A in the Restriction of Exo1-mediated DNA Break End Resection.The Journal of biological chemistry · 2015Article
- Article
- Structure of the Rad50 DNA double-strand break repair protein in complex with DNA.The EMBO journal · 2014Article
- To trim or not to trim: progression and control of DSB end resection.Cell cycle (Georgetown, Tex.) · 2013Article
- End-resection at DNA double-strand breaks in the three domains of life.Biochemical Society transactions · 2013Review
- MRE11 and RAD50, but not NBS1, are essential for gene targeting in the moss Physcomitrella patens.Nucleic acids research · 2012Article
- Regulatory networks integrating cell cycle control with DNA damage checkpoints and double-strand break repair.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2011Review
- Ku counteracts mobilization of PARP1 and MRN in chromatin damaged with DNA double-strand breaks.Nucleic acids research · 2011Article
- Polynucleotide phosphorylase exonuclease and polymerase activities on single-stranded DNA ends are modulated by RecN, SsbA and RecA proteins.Nucleic acids research · 2011Article
- Functional interplay of the Mre11 nuclease and Ku in the response to replication-associated DNA damage.Molecular and cellular biology · 2011Article
- Release of Ku and MRN from DNA ends by Mre11 nuclease activity and Ctp1 is required for homologous recombination repair of double-strand breaks.PLoS genetics · 2011Article
- Ku prevents Exo1 and Sgs1-dependent resection of DNA ends in the absence of a functional MRX complex or Sae2.The EMBO journal · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Yeast rad50 and mre11 nuclease mutants are hypersensitive to physical and chemical agents that induce DNA double-strand breaks (DSBs). This sensitivity was suppressed by elevating intracellular levels of TLC1, the RNA subunit of telomerase. Suppression required proteins linked to homologous recombination, including Rad51, Rad52, Rad59 and Exo1, but not genes of the nonhomologous end-joining (NHEJ) repair pathway. Deletion mutagenesis experiments demonstrated that the 5'-end of TLC1 RNA was essential and a segment containing a binding site for the Yku70/Yku80 complex was sufficient for suppression. A mutant TLC1 RNA unable to associate with Yku80 protein did not increase resistance. These and other genetic studies indicated that association of the Ku heterodimer with broken DNA ends inhibits recombination in mrx mutants, but not in repair-proficient cells or in other DNA repair single mutants. In support of this model, DNA damage resistance of mrx cells was enhanced when YKU70 was co-inactivated. Defective recombinational repair of DSBs in mrx cells thus arises from at least two separate processes: loss of Mrx nuclease-associated DNA end-processing and inhibition of the Exo1-mediated secondary recombination pathway by Ku.
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.