ReviewBiochemistry2016
Mutations for Worse or Better: Low-Fidelity DNA Synthesis by SOS DNA Polymerase V Is a Tightly Regulated Double-Edged Sword.
Review in Biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 43 citations in OpenAlex.
- Pyocyanin produced byAntimicrobial agents and chemotherapy · 2026Article
- The diverse phenotypic and mutational landscape induced by fluoroquinolone treatment.mSystems · 2025Article
- Exploring the Impact of Chemotherapy on the Emergence of Antibiotic Resistance in the Gut Microbiota of Colorectal Cancer Patients.Antibiotics (Basel, Switzerland) · 2025Review
- Escherichia coli DNA replication: the old model organism still holds many surprises.FEMS microbiology reviews · 2024Review
- CRISPR-Cas9-assisted genome editing inbioRxiv : the preprint server for biology · 2024Article
- Contribution of the SOS response and the DNA repair systems to norfloxacin induced mutations inMarine life science & technology · 2023Article
- Generation and Repair of Postreplication Gaps in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2023Review
- SOS-independent bacterial DNA damage responses: diverse mechanisms, unifying function.Current opinion in microbiology · 2023Review
- Mutate or die: Atomic structures explain bacterial SOS induction.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Structural basis for regulation of SOS response in bacteria.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- ATPase Activity of Bacillus subtilis RecA Affects the Dynamic Formation of RecA Filaments at DNA Double Strand Breaks.mSphere · 2022Article
- Sending out an SOS - the bacterial DNA damage response.Genetics and molecular biology · 2022Article
- The rarA gene as part of an expanded RecFOR recombination pathway: Negative epistasis and synthetic lethality with ruvB, recG, and recQ.PLoS genetics · 2021Article
- Non-canonical LexA proteins regulate the SOS response in the Bacteroidetes.Nucleic acids research · 2021Article
- ImuA Facilitates SOS Mutagenesis by Inhibiting RecA-Mediated Activity in Myxococcus xanthus.Applied and environmental microbiology · 2021Article
- Article
- Single-molecule live-cell imaging reveals RecB-dependent function of DNA polymerase IV in double strand break repair.Nucleic acids research · 2020Article
- Visualizing mutagenic repair: novel insights into bacterial translesion synthesis.FEMS microbiology reviews · 2020Review
- New complexities of SOS-induced "untargeted" mutagenesis in Escherichia coli as revealed by mutation accumulation and whole-genome sequencing.DNA repair · 2020Article
- Antibiotic-Induced Mutagenesis: Under the Microscope.Frontiers in microbiology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
1953, the year of Watson and Crick, bore witness to a less acclaimed yet highly influential discovery. Jean Weigle demonstrated that upon infection of Escherichia coli, λ phage deactivated by UV radiation, and thus unable to form progeny, could be reactivated by irradiation of the bacterial host. Evelyn Witkin and Miroslav Radman later revealed the presence of the SOS regulon. The more than 40 regulon genes are repressed by LexA protein and induced by the coproteolytic cleavage of LexA, catalyzed by RecA protein bound to single-stranded DNA, the RecA* nucleoprotein filament. Several SOS-induced proteins are engaged in repairing both cellular and extracellular damaged DNA. There's no "free lunch", however, because error-free repair is accompanied by error-prone translesion DNA synthesis (TLS), involving E. coli DNA polymerase V (UmuD'2C) and RecA*. This review describes the biochemical mechanisms of pol V-mediated TLS. pol V is active only as a mutasomal complex, pol V Mut = UmuD'2C-RecA-ATP. RecA* donates a single RecA subunit to pol V. We highlight three recent insights. (1) pol V Mut has an intrinsic DNA-dependent ATPase activity that governs polymerase binding and dissociation from DNA. (2) Active and inactive states of pol V Mut are determined at least in part by the distinct interactions between RecA and UmuC. (3) pol V is activated by RecA*, not at a blocked replisome, but at the inner cell membrane.
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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.