ArticlePloS one2013
The yeast Shu complex utilizes homologous recombination machinery for error-free lesion bypass via physical interaction with a Rad51 paralogue.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Rad51 determines pathway usage in post-replication repair.Nature communications · 2026Article
- Budding Yeast Ubiquitin Ligases Rad5 and Rad18 Bind a Novel PCNA Surface, which Is Required for their Functions in DNA-Damage Tolerance.International journal of biological sciences · 2026Article
- Rad51 filaments assembled in the absence of the complex formed by the Rad51 paralogs Rad55 and Rad57 are outcompeted by translesion DNA polymerases on UV-induced ssDNA gaps.PLoS genetics · 2023Article
- Standardization of Synthetic Biology Tools and Assembly Methods forACS synthetic biology · 2022Review
- The Shu complex prevents mutagenesis and cytotoxicity of single-strand specific alkylation lesions.eLife · 2021Article
- Review
- Genome Profiling for Aflatoxin BG3 (Bethesda, Md.) · 2020Article
- Effects of chain length and geometry on the activation of DNA damage bypass by polyubiquitylated PCNA.Nucleic acids research · 2020Article
- The Rad51 paralogs facilitate a novel DNA strand specific damage tolerance pathway.Nature communications · 2019Article
- RAD51D splice variants and cancer-associated mutations reveal XRCC2 interaction to be critical for homologous recombination.DNA repair · 2019Article
- Mapping DNA damage-dependent genetic interactions in yeast via party mating and barcode fusion genetics.Molecular systems biology · 2018Article
- Sgs1 helicase is required for efficient PCNA monoubiquitination and translesion DNA synthesis in Saccharomyces cerevisiae.Current genetics · 2018Article
- Structural basis for the functional role of the Shu complex in homologous recombination.Nucleic acids research · 2017Article
- Novel insights into RAD51 activity and regulation during homologous recombination and DNA replication.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2016Review
- The Shu complex promotes error-free tolerance of alkylation-induced base excision repair products.Nucleic acids research · 2016Article
- The Shu complex is a conserved regulator of homologous recombination.FEMS yeast research · 2016Article
- Review
- ThreeFrontiers in plant science · 2016Article
- Mechanism of DNA damage tolerance.World journal of biological chemistry · 2015Article
- Promotion of presynaptic filament assembly by the ensemble of S. cerevisiae Rad51 paralogues with Rad52.Nature communications · 2015Article
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7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA-damage tolerance (DDT) is defined as a mechanism by which eukaryotic cells resume DNA synthesis to fill the single-stranded DNA gaps left by replication-blocking lesions. Eukaryotic cells employ two different means of DDT, namely translesion DNA synthesis (TLS) and template switching, both of which are coordinately regulated through sequential ubiquitination of PCNA at the K164 residue. In the budding yeast Saccharomyces cerevisiae, the same PCNA-K164 residue can also be sumoylated, which recruits the Srs2 helicase to prevent undesired homologous recombination (HR). While the mediation of TLS by PCNA monoubiquitination has been extensively characterized, the method by which K63-linked PCNA polyubiquitination leads to template switching remains unclear. We recently identified a yeast heterotetrameric Shu complex that couples error-free DDT to HR as a critical step of template switching. Here we report that the Csm2 subunit of Shu physically interacts with Rad55, an accessory protein involved in HR. Rad55 and Rad57 are Rad51 paralogues and form a heterodimer to promote Rad51-ssDNA filament formation by antagonizing Srs2 activity. Although Rad55-Rad57 and Shu function in the same pathway and both act to inhibit Srs2 activity, Shu appears to be dedicated to error-free DDT while the Rad55-Rad57 complex is also involved in double-strand break repair. This study reveals the detailed steps of error-free lesion bypass and also brings to light an intrinsic interplay between error-free DDT and Srs2-mediated inhibition of HR.
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