ArticleJournal of bacteriology2012
Escherichia coli DNA polymerase IV (Pol IV), but not Pol II, dynamically switches with a stalled Pol III* replicase.
Article in Journal of bacteriology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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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
31 citing papers in PubMed.
- Thumb-domain dynamics modulate the functional repertoire of DNA-Polymerase IV (DinB).Nucleic acids research · 2023Article
- 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
- 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
- Peptides containing the PCNA interacting motif APIM bind to the β-clamp and inhibit bacterial growth and mutagenesis.Nucleic acids research · 2020Article
- Article
- Specialised DNA polymerases in Escherichia coli: roles within multiple pathways.Current genetics · 2018Review
- Oxygen and RNA in stress-induced mutation.Current genetics · 2018Review
- DNA polymerase IV primarily operates outside of DNA replication forks in Escherichia coli.PLoS genetics · 2018Article
- Single-molecule studies contrast ordered DNA replication with stochastic translesion synthesis.eLife · 2017Article
- Processing closely spaced lesions during Nucleotide Excision Repair triggers mutagenesis in E. coli.PLoS genetics · 2017Article
- Persistent damaged bases in DNA allow mutagenic break repair in Escherichia coli.PLoS genetics · 2017Article
- RNA Primer Extension Hinders DNA Synthesis byFrontiers in microbiology · 2017Article
- Mutations Affecting Potassium Import Restore the Viability of the Escherichia coli DNA Polymerase III holD Mutant.PLoS genetics · 2016Article
- DNA Polymerase III, but Not Polymerase IV, Must Be Bound to a τ-Containing DnaX Complex to Enable Exchange into Replication Forks.The Journal of biological chemistry · 2016Article
- Exchange between Escherichia coli polymerases II and III on a processivity clamp.Nucleic acids research · 2016Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
The dnaN159 allele encodes a temperature-sensitive mutant form of the β sliding clamp (β159). SOS-induced levels of DNA polymerase IV (Pol IV) confer UV sensitivity upon the dnaN159 strain, while levels of Pol IV ∼4-fold higher than those induced by the SOS response severely impede its growth. Here, we used mutations in Pol IV that disrupted specific interactions with the β clamp to test our hypothesis that these phenotypes were the result of Pol IV gaining inappropriate access to the replication fork via a Pol III*-Pol IV switch relying on both the rim and cleft of the clamp. Our results clearly demonstrate that Pol IV relied on both the clamp rim and cleft interactions for these phenotypes. In contrast to the case for Pol IV, elevated levels of the other Pols, including Pol II, which was expressed at levels ∼8-fold higher than the normal SOS-induced levels, failed to impede growth of the dnaN159 strain. These findings suggest that the mechanism used by Pol IV to switch with Pol III* is distinct from those used by the other Pols. Results of experiments utilizing purified components to reconstitute the Pol III*-Pol II switch in vitro indicated that Pol II switched equally well with both a stalled and an actively replicating Pol III* in a manner that was independent of the rim contact required by Pol IV. These results provide compelling support for the Pol III*-Pol IV two-step switch model and demonstrate important mechanistic differences in how Pol IV and Pol II switch with Pol III*.
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