ArticleThe Journal of biological chemistry2014
Rad52/Rad59-dependent recombination as a means to rectify faulty Okazaki fragment processing.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- The strand exchange domain of tumor suppressor PALB2 is intrinsically disordered and promotes oligomerization-dependent DNA compaction.iScience · 2024Article
- Effects of PCNA Stability on the Formation of Mutations.International journal of molecular sciences · 2024Article
- The strand exchange domain of tumor suppressor PALB2 is intrinsically disordered and promotes oligomerization-dependent DNA compaction.bioRxiv : the preprint server for biology · 2024Article
- Helicase activities of Rad5 and Rrm3 genetically interact in the prevention of recombinogenic DNA lesions in Saccharomyces cerevisiae.DNA repair · 2023Article
- Exploiting replication gaps for cancer therapy.Molecular cell · 2022Review
- The secondary-structured DNA-binding activity of Dna2 endonuclease/helicase is critical to cell growth under replication stress.The FEBS journal · 2021Article
- Recombineering and MAGE.Nature reviews. Methods primers · 2021Article
- FEN1 endonuclease as a therapeutic target for human cancers with defects in homologous recombination.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Article
- Review
- Rad52 Restrains Resection at DNA Double-Strand Break Ends in Yeast.Molecular cell · 2019Article
- Review
- Precise Editing at DNA Replication Forks Enables Multiplex Genome Engineering in Eukaryotes.Cell · 2017Article
- Article
- Transcription-replication conflicts at chromosomal fragile sites-consequences in M phase and beyond.Chromosoma · 2017Review
- SUMOylation of Rad52-Rad59 synergistically change the outcome of mitotic recombination.DNA repair · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The correct removal of 5'-flap structures by Rad27 and Dna2 during Okazaki fragment maturation is crucial for the stable maintenance of genetic materials and cell viability. In this study, we identified RAD52, a key recombination protein, as a multicopy suppressor of dna2-K1080E, a lethal helicase-negative mutant allele of DNA2 in yeasts. In contrast, the overexpression of Rad51, which works conjointly with Rad52 in canonical homologous recombination, failed to suppress the growth defect of the dna2-K1080E mutation, indicating that Rad52 plays a unique and distinct role in Okazaki fragment metabolism. We found that the recombination-defective Rad52-QDDD/AAAA mutant did not rescue dna2-K1080E, suggesting that Rad52-mediated recombination is important for suppression. The Rad52-mediated enzymatic stimulation of Dna2 or Rad27 is not a direct cause of suppression observed in vivo, as both Rad52 and Rad52-QDDD/AAAA proteins stimulated the endonuclease activities of both Dna2 and Rad27 to a similar extent. The recombination mediator activity of Rad52 was dispensable for the suppression, whereas both the DNA annealing activity and its ability to interact with Rad59 were essential. In addition, we found that several cohesion establishment factors, including Rsc2 and Elg1, were required for the Rad52-dependent suppression of dna2-K1080E. Our findings suggest a novel Rad52/Rad59-dependent, but Rad51-independent recombination pathway that could ultimately lead to the removal of faulty flaps in conjunction with cohesion establishment factors.
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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.