ArticleMutation research2011
Proofreading deficiency of Pol I increases the levels of spontaneous rpoB mutations in E. coli.
Article in Mutation research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 9 citations in OpenAlex.
- Novel Escherichia coli active site dnaE alleles with altered base and sugar selectivity.Molecular microbiology · 2021Article
- Determinants of Base-Pair Substitution Patterns Revealed by Whole-Genome Sequencing of DNA Mismatch Repair DefectiveGenetics · 2018Article
- Mutational Consequences of Ciprofloxacin in Escherichia coli.Antimicrobial agents and chemotherapy · 2016Article
- Investigating the mechanisms of ribonucleotide excision repair in Escherichia coli.Mutation research · 2014Article
- Competitive fitness during feast and famine: how SOS DNA polymerases influence physiology and evolution in Escherichia coli.Genetics · 2013Article
- DNA replication fidelity in Escherichia coli: a multi-DNA polymerase affair.FEMS microbiology reviews · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The fidelity role of DNA polymerase I in chromosomal DNA replication in E. coli was investigated using the rpoB forward target. These experiments indicated that in a strain carrying a proofreading-exonuclease-defective form of Pol I (polAexo mutant) the frequency of rpoB mutations increased by about 2-fold, consistent with a model that the fidelity of DNA polymerase I is important in controlling the overall fidelity of chromosomal DNA replication. DNA sequencing of rpoB mutants revealed that the Pol I exonuclease deficiency lead to an increase in a variety of base-substitution mutations. A polAexo mutator effect was also observed in strains defective in DNA mismatch repair and carrying the dnaE915 antimutator allele. Overall, the data are consistent with a proposed role of Pol I in the faithful completion of Okazaki fragment gaps at the replication fork.
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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.