ArticleMolecular and cellular biology2006
The rad51-K191R ATPase-defective mutant is impaired for presynaptic filament formation.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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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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
30 citing papers in PubMed, 44 citations in OpenAlex.
- Potential Rad54 separation of function mutation highlights unique roles during homologous recombination.PLoS genetics · 2026Article
- Mei5-Sae3 stabilizes both active and inactive forms of Dmc1 filaments independently of its impact on ATP hydrolysis.Nucleic acids research · 2025Article
- How strand exchange protein function benefits from ATP hydrolysis.Current opinion in genetics & development · 2021Review
- Review
- Srs2 and Pif1 as Model Systems for Understanding Sf1a and Sf1b Helicase Structure and Function.Genes · 2021Review
- The Rad51 paralog complex Rad55-Rad57 acts as a molecular chaperone during homologous recombination.Molecular cell · 2021Article
- Single-molecule visualization of human RECQ5 interactions with single-stranded DNA recombination intermediates.Nucleic acids research · 2021Article
- Emerging non-canonical roles for the Rad51-Rad52 interaction in response to double-strand breaks in yeast.Current genetics · 2020Review
- Microcephaly family protein MCPH1 stabilizes RAD51 filaments.Nucleic acids research · 2020Article
- Rad54 Drives ATP Hydrolysis-Dependent DNA Sequence Alignment during Homologous Recombination.Cell · 2020Article
- Interaction of yeast Rad51 and Rad52 relieves Rad52-mediated inhibition of de novo telomere addition.PLoS genetics · 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
- A Novel Cell-Penetrating Antibody Fragment Inhibits the DNA Repair Protein RAD51.Scientific reports · 2019Article
- The RecQ helicase Sgs1 drives ATP-dependent disruption of Rad51 filaments.Nucleic acids research · 2019Article
- Helicase Mechanisms During Homologous Recombination inAnnual review of biophysics · 2019Review
- Dissociation of Rad51 Presynaptic Complexes and Heteroduplex DNA Joints by Tandem Assemblies of Srs2.Cell reports · 2017Article
- RAD51 variant proteins from human lung and kidney tumors exhibit DNA strand exchange defects.DNA repair · 2016Article
- Caffeine inhibits gene conversion by displacing Rad51 from ssDNA.Nucleic acids research · 2015Article
- Functional Relationship of ATP Hydrolysis, Presynaptic Filament Stability, and Homologous DNA Pairing Activity of the Human Meiotic Recombinase DMC1.The Journal of biological chemistry · 2015Article
- Rad51 ATP binding but not hydrolysis is required to recruit Rad10 in synthesis-dependent strand annealing sites inAdvances in biological chemistry · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The nucleoprotein filament formed by Rad51 polymerization on single-stranded DNA is essential for homologous pairing and strand exchange. ATP binding is required for Rad51 nucleoprotein filament formation and strand exchange, but ATP hydrolysis is not required for these functions in vitro. Previous studies have shown that a yeast strain expressing the rad51-K191R allele is sensitive to ionizing radiation, suggesting an important role for ATP hydrolysis in vivo. The recruitment of Rad51-K191R to double-strand breaks is defective in vivo, and this phenotype can be suppressed by elimination of the Srs2 helicase, an antagonist of Rad51 filament formation. The phenotype of the rad51-K191R strain is also suppressed by overexpression of Rad54. In vitro, the Rad51-K191R protein exhibits a slight decrease in binding to DNA, consistent with the defect in presynaptic filament formation. However, the rad51-K191R mutation is dominant in heterozygous diploids, indicating that the defect is not due simply to reduced affinity for DNA. We suggest the Rad51-K191R protein either forms an altered filament or is defective in turnover, resulting in a reduced pool of free protein available for DNA binding.
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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.