ArticlePLoS genetics2015
A Genetic Selection for dinB Mutants Reveals an Interaction between DNA Polymerase IV and the Replicative Polymerase That Is Required for Translesion Synthesis.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 31 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
- 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
- A bipartite interaction with the processivity clamp potentiates Pol IV-mediated TLS.bioRxiv : the preprint server for biology · 2024Article
- Compartmentalization of the replication fork by single-stranded DNA-binding protein regulates translesion synthesis.Nature structural & molecular biology · 2022Article
- During Translesion Synthesis, Escherichia coli DinB89 (T120P) Alters Interactions of DinB (Pol IV) with Pol III Subunit Assemblies and SSB, but Not with the β Clamp.Journal of bacteriology · 2022Article
- Observing protein dynamics during DNA-lesion bypass by the replisome.Frontiers in molecular biosciences · 2022Review
- The Mutant βJournal of bacteriology · 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
- 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
- The SOS system: A complex and tightly regulated response to DNA damage.Environmental and molecular mutagenesis · 2019Review
- 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
- Characterization of a coupled DNA replication and translesion synthesis polymerase supraholoenzyme from archaea.Nucleic acids research · 2017Article
- Persistent damaged bases in DNA allow mutagenic break repair in Escherichia coli.PLoS genetics · 2017Article
- Sub-Minimum Inhibitory Concentrations of Rhubarb Water Extracts InhibitFrontiers in pharmacology · 2017Article
- DNA Polymerases ImuC and DinB Are Involved in DNA Alkylation Damage Tolerance in Pseudomonas aeruginosa and Pseudomonas putida.PloS one · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Translesion DNA synthesis (TLS) by specialized DNA polymerases (Pols) is a conserved mechanism for tolerating replication blocking DNA lesions. The actions of TLS Pols are managed in part by ring-shaped sliding clamp proteins. In addition to catalyzing TLS, altered expression of TLS Pols impedes cellular growth. The goal of this study was to define the relationship between the physiological function of Escherichia coli Pol IV in TLS and its ability to impede growth when overproduced. To this end, 13 novel Pol IV mutants were identified that failed to impede growth. Subsequent analysis of these mutants suggest that overproduced levels of Pol IV inhibit E. coli growth by gaining inappropriate access to the replication fork via a Pol III-Pol IV switch that is mechanistically similar to that used under physiological conditions to coordinate Pol IV-catalyzed TLS with Pol III-catalyzed replication. Detailed analysis of one mutant, Pol IV-T120P, and two previously described Pol IV mutants impaired for interaction with either the rim (Pol IVR) or the cleft (Pol IVC) of the β sliding clamp revealed novel insights into the mechanism of the Pol III-Pol IV switch. Specifically, Pol IV-T120P retained complete catalytic activity in vitro but, like Pol IVR and Pol IVC, failed to support Pol IV TLS function in vivo. Notably, the T120P mutation abrogated a biochemical interaction of Pol IV with Pol III that was required for Pol III-Pol IV switching. Taken together, these results support a model in which Pol III-Pol IV switching involves interaction of Pol IV with Pol III, as well as the β clamp rim and cleft. Moreover, they provide strong support for the view that Pol III-Pol IV switching represents a vitally important mechanism for regulating TLS in vivo by managing access of Pol IV to the DNA.
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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.