ArticleMolecular and cellular biology2012
Distinct roles of Mus81, Yen1, Slx1-Slx4, and Rad1 nucleases in the repair of replication-born double-strand breaks by sister chromatid exchange.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 51 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.
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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
51 citing papers in PubMed, 64 citations in OpenAlex.
- Analysis ofInternational journal of molecular sciences · 2025Article
- Review
- DNA damage checkpoint and repair: From the budding yeastComputational and structural biotechnology journal · 2021Review
- A novel function for CDK2 activity at meiotic crossover sites.PLoS biology · 2020Article
- Homologous recombination and Mus81 promote replication completion in response to replication fork blockage.EMBO reports · 2020Article
- Genomic Instability in Fungal Plant Pathogens.Genes · 2020Review
- Histone demethylase JMJD1A promotes expression of DNA repair factors and radio-resistance of prostate cancer cells.Cell death & disease · 2020Article
- ATR Protects the Genome against R Loops through a MUS81-Triggered Feedback Loop.Molecular cell · 2020Article
- Review
- A mutation in the endonuclease domain of mouse MLH3 reveals novel roles for MutLγ during crossover formation in meiotic prophase I.PLoS genetics · 2019Article
- Guidelines for DNA recombination and repair studies: Cellular assays of DNA repair pathways.Microbial cell (Graz, Austria) · 2019Review
- Review
- Slx5-Slx8 ubiquitin ligase targets active pools of the Yen1 nuclease to limit crossover formation.Nature communications · 2018Article
- Role of PCNA and RFC in promoting Mus81-complex activity.BMC biology · 2017Article
- Article
- Break induced replication in eukaryotes: mechanisms, functions, and consequences.Critical reviews in biochemistry and molecular biology · 2017Review
- Pathways and Mechanisms that Prevent Genome Instability inGenetics · 2017Review
- Substrate preference of Gen endonucleases highlights the importance of branched structures as DNA damage repair intermediates.Nucleic acids research · 2017Article
- SLX4 Prevents GEN1-Dependent DSBs During DNA Replication Arrest Under Pathological Conditions in Human Cells.Scientific reports · 2017Article
- Hypermutation signature reveals a slippage and realignment model of translesion synthesis by Rev3 polymerase in cisplatin-treated yeast.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Most spontaneous DNA double-strand breaks (DSBs) arise during replication and are repaired by homologous recombination (HR) with the sister chromatid. Many proteins participate in HR, but it is often difficult to determine their in vivo functions due to the existence of alternative pathways. Here we take advantage of an in vivo assay to assess repair of a specific replication-born DSB by sister chromatid recombination (SCR). We analyzed the functional relevance of four structure-selective endonucleases (SSEs), Yen1, Mus81-Mms4, Slx1-Slx4, and Rad1, on SCR in Saccharomyces cerevisiae. Physical and genetic analyses showed that ablation of any of these SSEs leads to a specific SCR decrease that is not observed in general HR. Our work suggests that Yen1, Mus81-Mms4, Slx4, and Rad1, but not Slx1, function independently in the cleavage of intercrossed DNA structures to reconstitute broken replication forks via HR with the sister chromatid. These unique effects, which have not been detected in other studies unless double mutant combinations were used, indicate the formation of distinct alternatives for the repair of replication-born DSBs that require specific SSEs.
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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.