ArticleGenetics2002
Saturation of DNA mismatch repair and error catastrophe by a base analogue in Escherichia coli.
Article in Genetics, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
The trial behind it
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
21 citing papers in PubMed, 42 citations in OpenAlex.
- Repair of single-strand breaks during the cell cycle - saturation of repair capacity.Nucleus (Austin, Tex.) · 2026Article
- Real-time monitoring of replication errors' fate reveals the origin and dynamics of spontaneous mutations.Nature communications · 2024Article
- Mismatch Repair: From Preserving Genome Stability to Enabling Mutation Studies in Real-Time Single Cells.Cells · 2021Review
- Transcription Factors as Evolvable Biosensors.Analytical sciences : the international journal of the Japan Society for Analytical Chemistry · 2021Review
- Real-time visualization of mutations and their fitness effects in single bacteria.Nature protocols · 2019Article
- Chloroethylating anticancer drug-induced mutagenesis and its repair inGenes and environment : the official journal of the Japanese Environmental Mutagen Society · 2019Article
- Article
- Transient MutS-Based Hypermutation System for Adaptive Evolution of Lactobacillus casei to Low pH.Applied and environmental microbiology · 2017Article
- Replacement of 2'-Deoxycytidine by 2'-Deoxycytidine Analogues in the E. coli Genome.Journal of the American Chemical Society · 2016Article
- Article
- Rapid and liquid-based selection of genetic switches using nucleoside kinase fused with aminoglycoside phosphotransferase.PloS one · 2015Article
- Hypermutability and error catastrophe due to defects in ribonucleotide reductase.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Distinct pathways for repairing mutagenic lesions induced by methylating and ethylating agents.Mutagenesis · 2013Article
- Genome-wide mutation avalanches induced in diploid yeast cells by a base analog or an APOBEC deaminase.PLoS genetics · 2013Article
- Mutational consequences of dNTP pool imbalances in E. coli.DNA repair · 2013Article
- Stoichiometry of MutS and MutL at unrepaired mismatches in vivo suggests a mechanism of repair.Nucleic acids research · 2012Article
- A nucleoside kinase as a dual selector for genetic switches and circuits.Nucleic acids research · 2011Article
- Optimization of DNA polymerase mutation rates during bacterial evolution.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Binding of MutS protein to oligonucleotides containing a methylated or an ethylated guanine residue, and correlation with mutation frequency.Mutation research · 2008Article
- 2-aminopurine allows interspecies recombination by a reversible inactivation of the Escherichia coli mismatch repair system.Journal of bacteriology · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deoxyribosyl-dihydropyrimido[4,5-c][1,2]oxazin-7-one (dP) is a potent mutagenic deoxycytidine-derived base analogue capable of pairing with both A and G, thereby causing G. C --> A. T and A. T --> G. C transition mutations. We have found that the Escherichia coli DNA mismatch-repair system can protect cells against this mutagenic action. At a low dose, dP is much more mutagenic in mismatch-repair-defective mutH, mutL, and mutS strains than in a wild-type strain. At higher doses, the difference between the wild-type and the mutator strains becomes small, indicative of saturation of mismatch repair. Introduction of a plasmid containing the E. coli mutL(+) gene significantly reduces dP-induced mutagenesis. Together, the results indicate that the mismatch-repair system can remove dP-induced replication errors, but that its capacity to remove dP-containing mismatches can readily be saturated. When cells are cultured at high dP concentration, mutant frequencies reach exceptionally high levels and viable cell counts are reduced. The observations are consistent with a hypothesis in which dP-induced cell killing and growth impairment result from excess mutations (error catastrophe), as previously observed spontaneously in proofreading-deficient mutD (dnaQ) strains.
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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.