ArticleGenetics2007
Brc1-mediated rescue of Smc5/6 deficiency: requirement for multiple nucleases and a novel Rad18 function.
Article in Genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- The SAGA histone acetyltransferase module targets SMC5/6 to specific genes.Epigenetics & chromatin · 2023Article
- Recruitment, loading, and activation of the Smc5-Smc6 SUMO ligase.Current genetics · 2019Review
- XPG-related nucleases are hierarchically recruited for double-stranded rDNA break resection.The Journal of biological chemistry · 2019Article
- Brc1 Promotes the Focal Accumulation and SUMO Ligase Activity of Smc5-Smc6 during Replication Stress.Molecular and cellular biology · 2019Article
- Multi-BRCT Domain Protein Brc1 Links Rhp18/Rad18 and γH2A To Maintain Genome Stability during S Phase.Molecular and cellular biology · 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
- Loss of Caenorhabditis elegans BRCA1 promotes genome stability during replication in smc-5 mutants.Genetics · 2014Article
- Associations of polymorphisms in DNA repair genes and MDR1 gene with chemotherapy response and survival of non-small cell lung cancer.PloS one · 2014Article
- Brc1 links replication stress response and centromere function.Cell cycle (Georgetown, Tex.) · 2013Review
- γH2A-binding protein Brc1 affects centromere function in fission yeast.Molecular and cellular biology · 2013Article
- Initiation of DNA damage responses through XPG-related nucleases.The EMBO journal · 2013Article
- Brc1-dependent recovery from replication stress.Journal of cell science · 2012Article
- The Smc complexes in DNA damage response.Cell & bioscience · 2012Article
- Nse1-dependent recruitment of Smc5/6 to lesion-containing loci contributes to the repair defects of mutant complexes.Molecular biology of the cell · 2011Article
- Schizosaccharomyces pombe Cds1Chk2 regulates homologous recombination at stalled replication forks through the phosphorylation of recombination protein Rad60.Journal of cell science · 2009Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Smc5/6 is a structural maintenance of chromosomes complex, related to the cohesin and condensin complexes. Recent studies implicate Smc5/6 as being essential for homologous recombination. Each gene is essential, but hypomorphic alleles are defective in the repair of a diverse array of lesions. A particular allele of smc6 (smc6-74) is suppressed by overexpression of Brc1, a six-BRCT domain protein that is required for DNA repair during S-phase. This suppression requires the postreplication repair (PRR) protein Rhp18 and the structure-specific endonucleases Slx1/4 and Mus81/Eme1. However, we show here that the contribution of Rhp18 is via a novel pathway that is independent of PCNA ubiquitination and PRR. Moreover, we identify Exo1 as an additional nuclease required for Brc1-mediated suppression of smc6-74, independent of mismatch repair. Further, the Apn2 endonuclease is required for the viability of smc6 mutants without extrinsic DNA damage, although this is not due to a defect in base excision repair. Several nucleotide excision repair genes are similarly shown to ensure viability of smc6 mutants. The requirement for excision factors for the viability of smc6 mutants is consistent with an inability to respond to spontaneous lesions by Smc5/6-dependent 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.