ArticleProceedings of the National Academy of Sciences of the United States of America2002
Alternate pathways involving Sgs1/Top3, Mus81/ Mms4, and Srs2 prevent formation of toxic recombination intermediates from single-stranded gaps created by DNA replication.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. 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 198 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
198 citing papers in PubMed, 320 citations in OpenAlex.
- The SOS response acts as a regulatory switch that balances helicase anti-recombination with transcription-replication conflict resolution activities in Escherichia coli.G3 (Bethesda, Md.) · 2026Article
- Synthetic rescue in Saccharomyces cerevisiae: Concepts, large-scale genetic mapping, and functional implications.Journal of microbiology (Seoul, Korea) · 2026Review
- A transient mutational burst occurs during yeast colony development.Molecular systems biology · 2025Article
- SRS2 is required for MUS81-dependent CO formation in zmm mutants.PLoS genetics · 2025Article
- Deep structure-function analysis of the endonuclease Mus81 with dominant mutational scanning.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Multifaceted roles of H2B mono-ubiquitylation in D-loop metabolism during homologous recombination repair.Nucleic acids research · 2025Article
- Nonhomologous tails direct heteroduplex rejection and mismatch correction during single-strand annealing in Saccharomyces cerevisiae.PLoS genetics · 2024Article
- Cellular Responses to Widespread DNA Replication Stress.International journal of molecular sciences · 2023Review
- Genetic inhibitors of APOBEC3B-induced mutagenesis.Genome research · 2023Article
- The Inability to Disassemble Rad51 Nucleoprotein Filaments Leads to Aberrant Mitosis and Cell Death.Biomedicines · 2023Article
- 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
- Roles of homologous recombination in response to ionizing radiation-induced DNA damage.International journal of radiation biology · 2023Review
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- Metnase and EEPD1: DNA Repair Functions and Potential Targets in Cancer Therapy.Frontiers in oncology · 2022Review
- Review
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- Smc5/6 functions with Sgs1-Top3-Rmi1 to complete chromosome replication at natural pause sites.Nature communications · 2021Article
- Behavior of dicentric chromosomes in budding yeast.PLoS genetics · 2021Article
- Origin, Regulation, and Fitness Effect of Chromosomal Rearrangements in the YeastInternational journal of molecular sciences · 2021Review
- The Safe Path at the Fork: Ensuring Replication-Associated DNA Double-Strand Breaks are Repaired by Homologous Recombination.Frontiers in genetics · 2021Review
138 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
Toxic recombination events are detected in vegetative Saccharomyces cerevisiae cells through negative growth interactions between certain combinations of mutations. For example, mutations affecting both the Srs2 and Sgs1 helicases result in extremely poor growth, a phenotype suppressed by mutations in genes that govern early stages of recombination. Here, we identify a similar interaction involving double mutations affecting Sgs1 or Top3 and Mus81 or Mms4. We also find that the primary DNA structures that initiate these toxic recombination events cannot be double-strand breaks and thus are likely to be single-stranded DNA. We interpret our results in the context of the idea that replication stalling leaves single-stranded DNA, which can then be processed by two competing mechanisms: recombination and nonrecombination gap-filling. Functions involved in preventing toxic recombination would either avoid replicative defects or act on recombination intermediates. Our results suggest that Srs2 channels recombination intermediates back into the gap-filling route, whereas Sgs1Top3 and Mus81Mms4 are involved in recombination andor in replication to allow replication restart.
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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.