ArticleProceedings of the National Academy of Sciences of the United States of America2013
Hypermutability and error catastrophe due to defects in ribonucleotide reductase.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
- Should I stay or should I go? DNA damage thresholds drive stay-or-go decisions inJournal of bacteriology · 2026Review
- Article
- Hypermutability ofEmerging microbes & infections · 2025Article
- 2.6-Å resolution cryo-EM structure of a class Ia ribonucleotide reductase trapped with mechanism-based inhibitor NProceedings of the National Academy of Sciences of the United States of America · 2024Article
- 2.6-Å resolution cryo-EM structure of a class Ia ribonucleotide reductase trapped with mechanism-based inhibitor NbioRxiv : the preprint server for biology · 2024Article
- Escherichia coli DNA replication: the old model organism still holds many surprises.FEMS microbiology reviews · 2024Review
- SAMHD1 restricts the deoxyguanosine triphosphate pool contributing to telomere stability in telomerase-positive cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Article
- IRBIT Directs Differentiation of Intestinal Stem Cell Progeny to Maintain Tissue Homeostasis.iScience · 2020Article
- Cyclin F-dependent degradation of E2F7 is critical for DNA repair and G2-phase progression.The EMBO journal · 2019Article
- Article
- High-throughput identification of the sensitivities of an Escherichia coli ΔrecA mutant strain to various chemical compounds.The Journal of antibiotics · 2019Article
- The Antibiotic Trimethoprim Displays Strong Mutagenic Synergy with 2-Aminopurine.Antimicrobial agents and chemotherapy · 2019Article
- A genetic screen pinpoints ribonucleotide reductase residues that sustain dNTP homeostasis and specifies a highly mutagenic type of dNTP imbalance.Nucleic acids research · 2019Article
- Periodic Variation of Mutation Rates in Bacterial Genomes Associated with Replication Timing.mBio · 2018Article
- Ribonucleotides incorporated by the yeast mitochondrial DNA polymerase are not repaired.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Yeast DNA polymerase ζ maintains consistent activity and mutagenicity across a wide range of physiological dNTP concentrations.Nucleic acids research · 2017Article
- Review
- Fluorescence-Based Reporters for Detection of Mutagenesis in E. coli.Methods in enzymology · 2017Article
- Mutagen Synergy: Hypermutability Generated by Specific Pairs of Base Analogs.Journal of bacteriology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The enzyme ribonucleotide reductase (RNR) plays a critical role in the production of deoxynucleoside-5'-triphosphates (dNTPs), the building blocks for DNA synthesis and replication. The levels of the cellular dNTPs are tightly controlled, in large part through allosteric control of RNR. One important reason for controlling the dNTPs relates to their ability to affect the fidelity of DNA replication and, hence, the cellular mutation rate. We have previously isolated a set of mutants of Escherichia coli RNR that are characterized by altered dNTP pools and increased mutation rates (mutator mutants). Here, we show that one particular set of RNR mutants, carrying alterations at the enzyme's allosteric specificity site, is characterized by relatively modest dNTP pool deviations but exceptionally strong mutator phenotypes, when measured in a mutational forward assay (>1,000-fold increases). We provide evidence indicating that this high mutability is due to a saturation of the DNA mismatch repair system, leading to hypermutability and error catastrophe. The results indicate that, surprisingly, even modest deviations of the cellular dNTP pools, particularly when the pool deviations promote particular types of replication errors, can have dramatic consequences for mutation rates.
Indexed as
Identifiers
What OpenQuestion holds
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.