ArticleNature structural & molecular biology2013
Preferential D-loop extension by a translesion DNA polymerase underlies error-prone recombination.
Article in Nature structural & molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
The trial behind it
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
25 citing papers in PubMed, 32 citations in OpenAlex.
- CRISPR-Cas9-mediated homology-directed repair for precise gene editing.Molecular therapy. Nucleic acids · 2024Review
- Precise genome-editing in human diseases: mechanisms, strategies and applications.Signal transduction and targeted therapy · 2024Review
- Age of Antibiotic Resistance in MDR/XDR Clinical Pathogen ofPharmaceuticals (Basel, Switzerland) · 2023Review
- Generation and Repair of Postreplication Gaps in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2023Review
- Stress-Induced Mutagenesis, Gambler Cells, and Stealth Targeting Antibiotic-Induced Evolution.mBio · 2022Review
- Targeting evolution of antibiotic resistance by SOS response inhibition.Computational and structural biotechnology journal · 2021Review
- Single-molecule live-cell imaging reveals RecB-dependent function of DNA polymerase IV in double strand break repair.Nucleic acids research · 2020Article
- Visualizing mutagenic repair: novel insights into bacterial translesion synthesis.FEMS microbiology reviews · 2020Review
- Role of RadA and DNA Polymerases in Recombination-Associated DNA Synthesis in Hyperthermophilic Archaea.Biomolecules · 2020Article
- Antibiotic-Induced Mutagenesis: Under the Microscope.Frontiers in microbiology · 2020Review
- Slow extension of the invading DNA strand in a D-loop formed by RecA-mediated homologous recombination may enhance recognition of DNA homology.The Journal of biological chemistry · 2019Article
- Residues in the fingers domain of the translesion DNA polymerase DinB enable its unique participation in error-prone double-strand break repair.The Journal of biological chemistry · 2019Article
- The SOS system: A complex and tightly regulated response to DNA damage.Environmental and molecular mutagenesis · 2019Review
- The positioning of Chi sites allows the RecBCD pathway to suppress some genomic rearrangements.Nucleic acids research · 2019Article
- Specialised DNA polymerases in Escherichia coli: roles within multiple pathways.Current genetics · 2018Review
- Article
- DNA polymerase IV primarily operates outside of DNA replication forks in Escherichia coli.PLoS genetics · 2018Article
- Single-molecule imaging reveals multiple pathways for the recruitment of translesion polymerases after DNA damage.Nature communications · 2017Article
- Collision with duplex DNA renders Escherichia coli DNA polymerase III holoenzyme susceptible to DNA polymerase IV-mediated polymerase switching on the sliding clamp.Scientific reports · 2017Article
- Persistent damaged bases in DNA allow mutagenic break repair in Escherichia coli.PLoS genetics · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Although homologous recombination is considered an accurate form of DNA repair, genetics suggest that the Escherichia coli translesion DNA polymerase IV (Pol IV, also known as DinB) promotes error-prone recombination during stress, which allows cells to overcome adverse conditions. However, how Pol IV functions and is regulated during recombination under stress is unknown. We show that Pol IV is highly proficient in error-prone recombination and is preferentially recruited to displacement loops (D loops) at stress-induced concentrations in vitro. We also found that high-fidelity Pol II switches to exonuclease mode at D loops, which is stimulated by topological stress and reduced deoxyribonucleotide pool concentration during stationary phase. The exonuclease activity of Pol II enables it to compete with Pol IV, which probably suppresses error-prone recombination. These findings indicate that preferential D-loop extension by Pol IV facilitates error-prone recombination and explain how Pol II reduces such errors in vivo.
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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.