ArticleGenetics2005
Brc1-mediated DNA repair and damage tolerance.
Article in Genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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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Who cites it
42 citing papers in PubMed.
- The BRCT Domain from the Homologue of the Oncogene PES1 inInternational journal of molecular sciences · 2022Article
- Nse5/6 is a negative regulator of the ATPase activity of the Smc5/6 complex.Nucleic acids research · 2021Article
- Genetic investigation of formaldehyde-induced DNA damage response in Schizosaccharomyces pombe.Current genetics · 2020Article
- Molecular Basis for Control of Diverse Genome Stability Factors by the Multi-BRCT Scaffold Rtt107.Molecular cell · 2019Article
- Recruitment, loading, and activation of the Smc5-Smc6 SUMO ligase.Current genetics · 2019Review
- Brc1 Promotes the Focal Accumulation and SUMO Ligase Activity of Smc5-Smc6 during Replication Stress.Molecular and cellular biology · 2019Article
- Histone H3 lysine 36 methyltransferase mobilizes NER factors to regulate tolerance against alkylation damage in fission yeast.Nucleic acids research · 2018Article
- Multi-BRCT Domain Protein Brc1 Links Rhp18/Rad18 and γH2A To Maintain Genome Stability during S Phase.Molecular and cellular biology · 2017Article
- Article
- Genetic controls of DNA damage avoidance in response to acetaldehyde in fission yeast.Cell cycle (Georgetown, Tex.) · 2017Article
- An acetyltransferase-independent function of Eso1 regulates centromere cohesion.Molecular biology of the cell · 2016Article
- Incision of damaged DNA in the presence of an impaired Smc5/6 complex imperils genome stability.Nucleic acids research · 2016Article
- Multi-BRCT scaffolds use distinct strategies to support genome maintenance.Cell cycle (Georgetown, Tex.) · 2016Review
- Resolving complex chromosome structures during meiosis: versatile deployment of Smc5/6.Chromosoma · 2016Review
- Critical Function of γH2A in S-Phase.PLoS genetics · 2015Article
- DNA repair. Proteomics reveals dynamic assembly of repair complexes during bypass of DNA cross-links.Science (New York, N.Y.) · 2015Article
- Genetic Interaction Landscape Reveals Critical Requirements for Schizosaccharomyces pombe Brc1 in DNA Damage Response Mutants.G3 (Bethesda, Md.) · 2015Article
- Ku stabilizes replication forks in the absence of Brc1.PloS one · 2015Article
- Loss of Caenorhabditis elegans BRCA1 promotes genome stability during replication in smc-5 mutants.Genetics · 2014Article
- TORC2 is required to maintain genome stability during S phase in fission yeast.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
The structural maintenance of chromosome (SMC) proteins are key elements in controlling chromosome dynamics. In eukaryotic cells, three essential SMC complexes have been defined: cohesin, condensin, and the Smc5/6 complex. The latter is essential for DNA damage responses; in its absence both repair and checkpoint responses fail. In fission yeast, the UV-C and ionizing radiation (IR) sensitivity of a specific hypomorphic allele encoding the Smc6 subunit, rad18-74 (renamed smc6-74), is suppressed by mild overexpression of a six-BRCT-domain protein, Brc1. Deletion of brc1 does not result in a hypersensitivity to UV-C or IR, and thus the function of Brc1 relative to the Smc5/6 complex has remained unclear. Here we show that brc1Delta cells are hypersensitive to a range of radiomimetic drugs that share the feature of creating lesions that are an impediment to the completion of DNA replication. Through a genetic analysis of brc1Delta epistasis and by defining genes required for Brc1 to suppress smc6-74, we find that Brc1 functions to promote recombination through a novel postreplication repair pathway and the structure-specific nucleases Slx1 and Mus81. Activation of this pathway through overproduction of Brc1 bypasses a repair defect in smc6-74, reestablishing resolution of lesions by recombination.
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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.