ArticleNucleic acids research2014
Enhancement of ADP release from the RAD51 presynaptic filament by the SWI5-SFR1 complex.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- RAD51AP1 is a versatile RAD51 modulator.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mei5-Sae3 stabilizes both active and inactive forms of Dmc1 filaments independently of its impact on ATP hydrolysis.Nucleic acids research · 2025Article
- SWI5-SFR1 reduces RAD51 recombinase extending units during filament assembly.Nucleic acids research · 2025Article
- The Swi5-Sfr1 complex regulates Dmc1- and Rad51-driven DNA strand exchange proceeding through two distinct three-stranded intermediates by different mechanisms.Nucleic acids research · 2024Article
- Hop2-Mnd1 and Swi5-Sfr1 stimulate Dmc1 filament assembly using distinct mechanisms.Nucleic acids research · 2023Article
- How strand exchange protein function benefits from ATP hydrolysis.Current opinion in genetics & development · 2021Review
- Nucleotide proofreading functions by nematode RAD51 paralogs facilitate optimal RAD51 filament function.Nature communications · 2021Article
- A novel motif of Rad51 serves as an interaction hub for recombination auxiliary factors.eLife · 2021Article
- Microcephaly family protein MCPH1 stabilizes RAD51 filaments.Nucleic acids research · 2020Article
- Real-time tracking reveals catalytic roles for the two DNA binding sites of Rad51.Nature communications · 2020Article
- Cooperative interactions facilitate stimulation of Rad51 by the Swi5-Sfr1 auxiliary factor complex.eLife · 2020Article
- A mutant form of Dmc1 that bypasses the requirement for accessory protein Mei5-Sae3 reveals independent activities of Mei5-Sae3 and Rad51 in Dmc1 filament stability.PLoS genetics · 2019Article
- Weaving DNA strands: structural insight on ATP hydrolysis in RecA-induced homologous recombination.Nucleic acids research · 2019Article
- Swi5-Sfr1 stimulates Rad51 recombinase filament assembly by modulating Rad51 dissociation.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Homologous recombination and the repair of DNA double-strand breaks.The Journal of biological chemistry · 2018Review
- Stable Nuclei of Nucleoprotein Filament and High ssDNA Binding Affinity Contribute to Enhanced RecA E38K Recombinase Activity.Scientific reports · 2017Article
- RecA-SSB Interaction Modulates RecA Nucleoprotein Filament Formation on SSB-Wrapped DNA.Scientific reports · 2017Article
- Review
- The β-isoform of BCCIP promotes ADP release from the RAD51 presynaptic filament and enhances homologous DNA pairing.Nucleic acids research · 2017Article
- Role of the RAD51-SWI5-SFR1 Ensemble in homologous recombination.Nucleic acids research · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Homologous recombination catalyzed by the RAD51 recombinase eliminates deleterious DNA lesions from the genome. In the presence of ATP, RAD51 forms a nucleoprotein filament on single-stranded DNA, termed the presynaptic filament, to initiate homologous recombination-mediated DNA double-strand break repair. The SWI5-SFR1 complex stabilizes the presynaptic filament and enhances its ability to mediate the homologous DNA pairing reaction. Here we characterize the RAD51 presynaptic filament stabilization function of the SWI5-SFR1 complex using optical tweezers. Biochemical experiments reveal that SWI5-SFR1 enhances ATP hydrolysis by single-stranded DNA-bound RAD51. Importantly, we show that SWI5-SFR1 acts by facilitating the release of ADP from the presynaptic filament. Our results thus provide mechanistic understanding of the function of SWI5-SFR1 in RAD51-mediated DNA 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.