ArticlePLoS genetics2018
DNA polymerase IV primarily operates outside of DNA replication forks in Escherichia coli.
Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 79 citations in OpenAlex.
- Genetic dissection of DNA damage tolerance in Bacillus subtilis: RecA and recombination functions regulate translesion synthesis.Nucleic acids research · 2026Article
- The SOS Response: A Double-Edged Sword between the Persister and Resister Formation.ACS omega · 2026Review
- Mechanisms of chromosomal DNA replication in Escherichia coli and Bacillus subtilis.FEMS microbiology reviews · 2026Review
- The RecBC complex protects single-stranded DNA gaps during lesion bypass.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Hallmarks of DNA replication stress responses in Escherichia coli and Bacillus subtilis.FEMS microbiology reviews · 2025Review
- Insight into Single-Molecule Imaging Techniques for the Study of Prokaryotic Genome Maintenance.Chemical & biomedical imaging · 2024Review
- The translesion polymerase Pol Y1 is a constitutive component of the B. subtilis replication machinery.Nucleic acids research · 2024Article
- Dysregulated DnaB unwinding induces replisome decoupling and daughter strand gaps that are countered by RecA polymerization.Nucleic acids research · 2024Article
- Escherichia coli DNA replication: the old model organism still holds many surprises.FEMS microbiology reviews · 2024Review
- SOS genes are rapidly induced while translesion synthesis polymerase activity is temporally regulated.Frontiers in microbiology · 2024Article
- Taxonomic Identification of the Arctic StrainInternational journal of molecular sciences · 2023Article
- Generation and Repair of Postreplication Gaps in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2023Review
- RecF protein targeting to post-replication (daughter strand) gaps II: RecF interaction with replisomes.Nucleic acids research · 2023Article
- Highly mismatch-tolerant homology testing by RecA could explain how homology length affects recombination.PloS one · 2023Article
- Replication stalling activates SSB for recruitment of DNA damage tolerance factors.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Direct visualization of translesion DNA synthesis polymerase IV at the replisome.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Compartmentalization of the replication fork by single-stranded DNA-binding protein regulates translesion synthesis.Nature structural & molecular biology · 2022Article
- Single strand gap repair: The presynaptic phase plays a pivotal role in modulating lesion tolerance pathways.PLoS genetics · 2022Article
- Observing protein dynamics during DNA-lesion bypass by the replisome.Frontiers in molecular biosciences · 2022Review
- Dynamics of Proteins and Macromolecular Machines in Escherichia coli.EcoSal Plus · 2021Review
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
In Escherichia coli, damage to the chromosomal DNA induces the SOS response, setting in motion a series of different DNA repair and damage tolerance pathways. DNA polymerase IV (pol IV) is one of three specialised DNA polymerases called into action during the SOS response to help cells tolerate certain types of DNA damage. The canonical view in the field is that pol IV primarily acts at replisomes that have stalled on the damaged DNA template. However, the results of several studies indicate that pol IV also acts on other substrates, including single-stranded DNA gaps left behind replisomes that re-initiate replication downstream of a lesion, stalled transcription complexes and recombination intermediates. In this study, we use single-molecule time-lapse microscopy to directly visualize fluorescently labelled pol IV in live cells. We treat cells with the DNA-damaging antibiotic ciprofloxacin, Methylmethane sulfonate (MMS) or ultraviolet light and measure changes in pol IV concentrations and cellular locations through time. We observe that only 5-10% of foci induced by DNA damage form close to replisomes, suggesting that pol IV predominantly carries out non-replisomal functions. The minority of foci that do form close to replisomes exhibit a broad distribution of colocalisation distances, consistent with a significant proportion of pol IV molecules carrying out postreplicative TLS in gaps behind the replisome. Interestingly, the proportion of pol IV foci that form close to replisomes drops dramatically in the period 90-180 min after treatment, despite pol IV concentrations remaining relatively constant. In an SOS-constitutive mutant that expresses high levels of pol IV, few foci are observed in the absence of damage, indicating that within cells access of pol IV to DNA is dependent on the presence of damage, as opposed to concentration-driven competition for binding sites.
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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.