ArticleJournal of bacteriology2004
The Escherichia coli dnaN159 mutant displays altered DNA polymerase usage and chronic SOS induction.
Article in Journal of bacteriology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 51 citations in OpenAlex.
- The loop domains of the E. coli β sliding clamp are required for Hda-dependent inactivation of DnaA.Genetics · 2026Article
- Phage-encoded small RNA hijacks host replication machinery to support the phage lytic cycle.Molecular cell · 2025Article
- Long-Range Destabilizing Effects of Mutations at theBiochemistry · 2025Article
- Roles for theJournal of biological rhythms · 2023Article
- 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
- Elevated Levels of the Escherichia coliJournal of bacteriology · 2021Article
- The Mutant βJournal of bacteriology · 2021Article
- Binding of the regulatory domain of MutL to the sliding β-clamp is species specific.Nucleic acids research · 2019Article
- Insufficient levels of the nrdAB-encoded ribonucleotide reductase underlie the severe growth defect of the Δhda E. coli strain.Molecular microbiology · 2017Article
- A Genetic Selection for dinB Mutants Reveals an Interaction between DNA Polymerase IV and the Replicative Polymerase That Is Required for Translesion Synthesis.PLoS genetics · 2015Article
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- Fate of the replisome following arrest by UV-induced DNA damage in Escherichia coli.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
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- Stress-induced mutation via DNA breaks in Escherichia coli: a molecular mechanism with implications for evolution and medicine.BioEssays : news and reviews in molecular, cellular and developmental biology · 2012Article
- Evidence for roles of the Escherichia coli Hda protein beyond regulatory inactivation of DnaA.Molecular microbiology · 2012Article
- Cellular characterization of the primosome and rep helicase in processing and restoration of replication following arrest by UV-induced DNA damage in Escherichia coli.Journal of bacteriology · 2012Article
- Escherichia coli DNA polymerase IV (Pol IV), but not Pol II, dynamically switches with a stalled Pol III* replicase.Journal of bacteriology · 2012Article
- A single hydrophobic cleft in the Escherichia coli processivity clamp is sufficient to support cell viability and DNA damage-induced mutagenesis in vivo.BMC molecular biology · 2010Article
- Mutations in the Bacillus subtilis beta clamp that separate its roles in DNA replication from mismatch repair.Journal of bacteriology · 2010Article
Corrections and comments
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1 author at 1 institution in 1 country.
Funding
Abstract
The Escherichia coli beta sliding clamp, which is encoded by the dnaN gene, is reported to interact with a variety of proteins involved in different aspects of DNA metabolism. Recent findings indicate that many of these partner proteins interact with a common surface on the beta clamp, suggesting that competition between these partners for binding to the clamp might help to coordinate both the nature and order of the events that take place at a replication fork. The purpose of the experiments discussed in this report was to test a prediction of this model, namely, that a mutant beta clamp protein impaired for interactions with the replicative DNA polymerase (polymerase III [Pol III]) would likewise have impaired interactions with other partner proteins and hence would display pleiotropic phenotypes. Results discussed herein indicate that the dnaN159-encoded mutant beta clamp protein (beta159) is impaired for interactions with the alpha catalytic subunit of Pol III. Moreover, the dnaN159 mutant strain displayed multiple replication and repair phenotypes, including sensitivity to UV light, an absolute dependence on the polymerase activity of Pol I for viability, enhanced Pol V-dependent mutagenesis, and altered induction of the global SOS response. Furthermore, epistasis analyses indicated that the UV sensitivity of the dnaN159 mutant was suppressed by (not epistatic with) inactivation of Pol IV (dinB gene product). Taken together, these findings suggest that in the dnaN159 mutant, DNA polymerase usage, and hence DNA replication, repair, and translesion synthesis, are altered. These findings are discussed in terms of a model to describe how the beta clamp might help to coordinate protein traffic at the replication fork.
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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.