ArticleThe Journal of biological chemistry2014
Replisome-mediated translesion synthesis and leading strand template lesion skipping are competing bypass mechanisms.
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 27 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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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
27 citing papers in PubMed, 40 citations in OpenAlex.
- A bipartite interaction with the processivity clamp potentiates Pol IV-mediated TLS.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mechanisms of DNA repair and mutagenesis induced by acetaldehyde, acrolein, aristolochic acids, and vinyl chloride.Journal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025Review
- Article
- Generation and Repair of Postreplication Gaps in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2023Review
- 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
- Changes in the architecture and abundance of replication intermediates delineate the chronology of DNA damage tolerance pathways at UV-stalled replication forks in human cells.Nucleic acids research · 2022Article
- Observing protein dynamics during DNA-lesion bypass by the replisome.Frontiers in molecular biosciences · 2022Review
- RecA-independent recombination: Dependence on the Escherichia coli RarA protein.Molecular microbiology · 2021Article
- Article
- A hand-off of DNA between archaeal polymerases allows high-fidelity replication to resume at a discrete intermediate three bases past 8-oxoguanine.Nucleic acids research · 2020Article
- Visualizing mutagenic repair: novel insights into bacterial translesion synthesis.FEMS microbiology reviews · 2020Review
- Two components of DNA replication-dependent LexA cleavage.The Journal of biological chemistry · 2020Article
- Frequent template switching in postreplication gaps: suppression of deleterious consequences by the Escherichia coli Uup and RadD proteins.Nucleic acids research · 2020Article
- A gatekeeping function of the replicative polymerase controls pathway choice in the resolution of lesion-stalled replisomes.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Replisome structure suggests mechanism for continuous fork progression and post-replication repair.DNA repair · 2019Review
- The SOS system: A complex and tightly regulated response to DNA damage.Environmental and molecular mutagenesis · 2019Review
- The recombination mediator proteins RecFOR maintain RecA* levels for maximal DNA polymerase V Mut activity.The Journal of biological chemistry · 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
- Replisome-mediated translesion synthesis by a cellular replicase.The Journal of biological chemistry · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A number of different enzymatic pathways have evolved to ensure that DNA replication can proceed past template base damage. These pathways include lesion skipping by the replisome, replication fork regression followed by either correction of the damage and origin-independent replication restart or homologous recombination-mediated restart of replication downstream of the lesion, and bypass of the damage by a translesion synthesis DNA polymerase. We report here that of two translesion synthesis polymerases tested, only DNA polymerase IV, not DNA polymerase II, could engage productively with the Escherichia coli replisome to bypass leading strand template damage, despite the fact that both enzymes are shown to be interacting with the replicase. Inactivation of the 3' → 5' proofreading exonuclease of DNA polymerase II did not enable bypass. Bypass by DNA polymerase IV required its ability to interact with the β clamp and act as a translesion polymerase but did not require its "little finger" domain, a secondary region of interaction with the β clamp. Bypass by DNA polymerase IV came at the expense of the inherent leading strand lesion skipping activity of the replisome, indicating that they are competing reactions.
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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.