ArticleNucleic acids research2016
Ctp1-dependent clipping and resection of DNA double-strand breaks by Mre11 endonuclease complex are not genetically separable.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 20 citations in OpenAlex.
- Pathogenic variants in MAEA disrupt DNA replication fork stability and are associated with developmental abnormalities in humans.Science advances · 2025Article
- To cleave or not and how? The DNA exonucleases and endonucleases in immunity.Genes & diseases · 2025Review
- Multi-step processing of replication stress-derived nascent strand DNA gaps by MRE11 and EXO1 nucleases.Nature communications · 2023Article
- PRMT1 and PRMT5: on the road of homologous recombination and non-homologous end joining.Genome instability & disease · 2023Article
- SIAH2 regulates DNA end resection and replication fork recovery by promoting CtIP ubiquitination.Nucleic acids research · 2022Article
- The KU-PARP14 axis differentially regulates DNA resection at stalled replication forks by MRE11 and EXO1.Nature communications · 2022Article
- A conserved Ctp1/CtIP C-terminal peptide stimulates Mre11 endonuclease activity.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Mre11 complex links sister chromatids to promote repair of a collapsed replication fork.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- The MRE11-RAD50-NBS1 Complex Conducts the Orchestration of Damage Signaling and Outcomes to Stress in DNA Replication and Repair.Annual review of biochemistry · 2018Review
- RNase H eliminates R-loops that disrupt DNA replication but is nonessential for efficient DSB repair.EMBO reports · 2018Article
- Rev7 and 53BP1/Crb2 prevent RecQ helicase-dependent hyper-resection of DNA double-strand breaks.eLife · 2018Article
- Genetic Separation of Sae2 Nuclease Activity from Mre11 Nuclease Functions in Budding Yeast.Molecular and cellular biology · 2017Article
- The end-joining factor Ku acts in the end-resection of double strand break-free arrested replication forks.Nature communications · 2017Article
- Lingering single-strand breaks trigger Rad51-independent homology-directed repair of collapsed replication forks in the polynucleotide kinase/phosphatase mutant of fission yeast.PLoS genetics · 2017Article
- CtIP/Ctp1/Sae2, molecular form fit for function.DNA repair · 2017Review
- Coordinated nuclease activities counteract Ku at single-ended DNA double-strand breaks.Nature communications · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Homologous recombination (HR) repair of programmed meiotic double-strand breaks (DSBs) requires endonucleolytic clipping of Rec12(Spo11)-oligonucleotides from 5' DNA ends followed by resection to generate invasive 3' single-stranded DNA tails. The Mre11-Rad50-Nbs1 (MRN) endonuclease and Ctp1 (CtIP and Sae2 ortholog) are required for both activities in fission yeast but whether they are genetically separable is controversial. Here, we investigate the mitotic DSB repair properties of Ctp1 C-terminal domain (ctp1-CD) mutants that were reported to be specifically clipping deficient. These mutants are sensitive to many clastogens, including those that create DSBs devoid of covalently bound proteins. These sensitivities are suppressed by genetically eliminating Ku nonhomologous end-joining (NHEJ) protein, indicating that Ctp1-dependent clipping by MRN is required for Ku removal from DNA ends. However, this rescue requires Exo1 resection activity, implying that Ctp1-dependent resection by MRN is defective in ctp1-CD mutants. The ctp1-CD mutants tolerate one but not multiple broken replication forks, and they are highly reliant on the Chk1-mediated cell cycle checkpoint arrest, indicating that HR repair is inefficient. We conclude that the C-terminal domain of Ctp1 is required for both efficient clipping and resection of DSBs by MRN and these activities are mechanistically similar.
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.