ArticleNucleic acids research2016
The Shu complex promotes error-free tolerance of alkylation-induced base excision repair products.
Article in Nucleic acids research, 2016. 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 20 papers.
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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
20 citing papers in PubMed, 30 citations in OpenAlex.
- The Yeast HMGB Protein Hmo1 Is a Multifaceted Regulator of DNA Damage Tolerance.International journal of molecular sciences · 2025Article
- A Rfa1-MN-based system reveals new factors involved in the rescue of broken replication forks.PLoS genetics · 2025Article
- The human Shu complex promotes RAD51 activity by modulating RPA dynamics on ssDNA.Nature communications · 2024Article
- Genetic inhibitors of APOBEC3B-induced mutagenesis.Genome research · 2023Article
- Human and bacterial TatD enzymes exhibit apurinic/apyrimidinic (AP) endonuclease activity.Nucleic acids research · 2023Article
- Hrq1/RECQL4 regulation is critical for preventing aberrant recombination during DNA intrastrand crosslink repair and is upregulated in breast cancer.PLoS genetics · 2022Article
- RAD51 paralog function in replicative DNA damage and tolerance.Current opinion in genetics & development · 2021Review
- The Shu complex prevents mutagenesis and cytotoxicity of single-strand specific alkylation lesions.eLife · 2021Article
- Regulation of RAD51 at the Transcriptional and Functional Levels: What Prospects for Cancer Therapy?Cancers · 2021Review
- Review
- Genome Profiling for Aflatoxin BG3 (Bethesda, Md.) · 2020Article
- New insights into abasic site repair and tolerance.DNA repair · 2020Review
- The human Shu complex functions with PDS5B and SPIDR to promote homologous recombination.Nucleic acids research · 2019Article
- 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
- RAD-ical New Insights into RAD51 Regulation.Genes · 2018Review
- Mapping DNA damage-dependent genetic interactions in yeast via party mating and barcode fusion genetics.Molecular systems biology · 2018Article
- Structural basis for the functional role of the Shu complex in homologous recombination.Nucleic acids research · 2017Article
- The Shu complex is a conserved regulator of homologous recombination.FEMS yeast research · 2016Article
- Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Here, we investigate the role of the budding yeast Shu complex in promoting homologous recombination (HR) upon replication fork damage. We recently found that the Shu complex stimulates Rad51 filament formation during HR through its physical interactions with Rad55-Rad57. Unlike other HR factors, Shu complex mutants are primarily sensitive to replicative stress caused by MMS and not to more direct DNA breaks. Here, we uncover a novel role for the Shu complex in the repair of specific MMS-induced DNA lesions and elucidate the interplay between HR and translesion DNA synthesis. We find that the Shu complex promotes high-fidelity bypass of MMS-induced alkylation damage, such as N3-methyladenine, as well as bypassing the abasic sites generated after Mag1 removes N3-methyladenine lesions. Furthermore, we find that the Shu complex responds to ssDNA breaks generated in cells lacking the abasic site endonucleases. At each lesion, the Shu complex promotes Rad51-dependent HR as the primary repair/tolerance mechanism over error-prone translesion DNA polymerases. Together, our work demonstrates that the Shu complex's promotion of Rad51 pre-synaptic filaments is critical for high-fidelity bypass of multiple replication-blocking lesion.
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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.