ArticleJournal of bacteriology2015
Interactions and Localization of Escherichia coli Error-Prone DNA Polymerase IV after DNA Damage.
Article in Journal of bacteriology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 25 citations in OpenAlex.
- The B. subtilis translesion polymerase Pol Y1 is not strongly recruited to sites of replication upon different types of DNA damage.PLoS genetics · 2026Article
- "ThebioRxiv : the preprint server for biology · 2026Article
- Integration of transcriptomic and proteomic analyses of cold shock response in Kosmotoga olearia, a typical thermophile with an incredible minimum growth temperature at 20 °C.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2022Article
- Dynamics of Proteins and Macromolecular Machines in Escherichia coli.EcoSal Plus · 2021Review
- RecA-independent recombination: Dependence on the Escherichia coli RarA protein.Molecular microbiology · 2021Article
- 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
- CRISPR/Cas9 recombineering-mediated deep mutational scanning of essential genes in Escherichia coli.Molecular systems biology · 2020Article
- Article
- Antibiotic-Induced Mutagenesis: Under the Microscope.Frontiers in microbiology · 2020Review
- Replication fidelity in E. coli: Differential leading and lagging strand effects for dnaE antimutator alleles.DNA repair · 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
- 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
- The DnaE polymerase from Deinococcus radiodurans features RecA-dependent DNA polymerase activity.Bioscience reports · 2016Article
- MutS regulates access of the error-prone DNA polymerase Pol IV to replication sites: a novel mechanism for maintaining replication fidelity.Nucleic acids research · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledEscherichia coli's DNA polymerase IV (Pol IV/DinB), a member of the Y family of error-prone polymerases, is induced during the SOS response to DNA damage and is responsible for translesion bypass and adaptive (stress-induced) mutation. In this study, the localization of Pol IV after DNA damage was followed using fluorescent fusions. After exposure of E. coli to DNA-damaging agents, fluorescently tagged Pol IV localized to the nucleoid as foci. Stepwise photobleaching indicated ∼60% of the foci consisted of three Pol IV molecules, while ∼40% consisted of six Pol IV molecules. Fluorescently tagged Rep, a replication accessory DNA helicase, was recruited to the Pol IV foci after DNA damage, suggesting that the in vitro interaction between Rep and Pol IV reported previously also occurs in vivo. Fluorescently tagged RecA also formed foci after DNA damage, and Pol IV localized to them. To investigate if Pol IV localizes to double-strand breaks (DSBs), an I-SceI endonuclease-mediated DSB was introduced close to a fluorescently labeled LacO array on the chromosome. After DSB induction, Pol IV localized to the DSB site in ∼70% of SOS-induced cells. RecA also formed foci at the DSB sites, and Pol IV localized to the RecA foci. These results suggest that Pol IV interacts with RecA in vivo and is recruited to sites of DSBs to aid in the restoration of DNA replication. IMPORTANCE: DNA polymerase IV (Pol IV/DinB) is an error-prone DNA polymerase capable of bypassing DNA lesions and aiding in the restart of stalled replication forks. In this work, we demonstrate in vivo localization of fluorescently tagged Pol IV to the nucleoid after DNA damage and to DNA double-strand breaks. We show colocalization of Pol IV with two proteins: Rep DNA helicase, which participates in replication, and RecA, which catalyzes recombinational repair of stalled replication forks. Time course experiments suggest that Pol IV recruits Rep and that RecA recruits Pol IV. These findings provide in vivo evidence that Pol IV aids in maintaining genomic stability not only by bypassing DNA lesions but also by participating in the restoration of stalled replication forks.
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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.