ArticlePLoS genetics2011
Unexpected role for Helicobacter pylori DNA polymerase I as a source of genetic variability.
Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 41 citations in OpenAlex.
- Review
- Translesion DNA synthesis on pyrimidine dimers by plant organellar DNA polymerases is metal-dependent.Nucleic acids research · 2026Article
- DNA polymerase I: structure, activity, and function in bacterial DNA replication and repair.Critical reviews in biochemistry and molecular biology · 2026Review
- Diversity and distribution of bacterial DNA polymerases.Nucleic acids research · 2026Article
- Correlation versus causation:mSphere · 2026Article
- Enhancement of Gastric Mucosal Defense by Phytomedicine in the Context ofBiologics : targets & therapy · 2026Review
- Genome-wide accumulations of non-random adaptive point mutations drive westward evolution of Helicobacter pylori.BMC microbiology · 2025Article
- Genomic epidemiology ofFrontiers in microbiology · 2025Article
- Molecular insights into the fine-tuning of pH-dependent ArsR-mediated regulation of the SabA adhesin in Helicobacter pylori.Nucleic acids research · 2024Article
- Inhibitors against DNA Polymerase I Family of Enzymes: Novel Targets and Opportunities.Biology · 2024Review
- High-Salt Diet ExacerbatesJournal of personalized medicine · 2023Review
- Whole Genome Sequencing for StudyingAntibiotics (Basel, Switzerland) · 2023Article
- Helicobacter pylori infection.Nature reviews. Disease primers · 2023Review
- Helicobacter pylori diversification during chronic infection within a single host generates sub-populations with distinct phenotypes.PLoS pathogens · 2020Article
- Article
- A novel taxon selection method, aimed at minimizing recombination, clarifies the discovery of a new sub-population ofEvolutionary applications · 2020Article
- Helicobacter pylori gene silencing in vivo demonstrates urease is essential for chronic infection.PLoS pathogens · 2017Article
- Polyamine- and NADPH-dependent generation of ROS during Helicobacter pylori infection: A blessing in disguise.Free radical biology & medicine · 2017Review
- Quantum changes in Helicobacter pylori gene expression accompany host-adaptation.DNA research : an international journal for rapid publication of reports on genes and genomes · 2017Article
- ComB proteins expression levels determine Helicobacter pylori competence capacity.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
Helicobacter pylori, a human pathogen infecting about half of the world population, is characterised by its large intraspecies variability. Its genome plasticity has been invoked as the basis for its high adaptation capacity. Consistent with its small genome, H. pylori possesses only two bona fide DNA polymerases, Pol I and the replicative Pol III, lacking homologues of translesion synthesis DNA polymerases. Bacterial DNA polymerases I are implicated both in normal DNA replication and in DNA repair. We report that H. pylori DNA Pol I 5'- 3' exonuclease domain is essential for viability, probably through its involvement in DNA replication. We show here that, despite the fact that it also plays crucial roles in DNA repair, Pol I contributes to genomic instability. Indeed, strains defective in the DNA polymerase activity of the protein, although sensitive to genotoxic agents, display reduced mutation frequencies. Conversely, overexpression of Pol I leads to a hypermutator phenotype. Although the purified protein displays an intrinsic fidelity during replication of undamaged DNA, it lacks a proofreading activity, allowing it to efficiently elongate mismatched primers and perform mutagenic translesion synthesis. In agreement with this finding, we show that the spontaneous mutator phenotype of a strain deficient in the removal of oxidised pyrimidines from the genome is in part dependent on the presence of an active DNA Pol I. This study provides evidence for an unexpected role of DNA polymerase I in generating genomic plasticity.
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