ArticleGene2005
Genetic analysis of the requirements for SOS induction by nalidixic acid in Escherichia coli.
Article in Gene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Synthetic lethal mutants inJournal of bacteriology · 2023Pooled it
- Escherichia coli type I toxin TisB exclusively controls proton depolarization following antibiotic induced DNA damage.Scientific reports · 2025Article
- Insights into antibiotic resistance promoted by quinolone exposure.Antimicrobial agents and chemotherapy · 2025Article
- A three-colour stress biosensor reveals multimodal response in single cells and spatiotemporal dynamics of biofilms.NPJ biofilms and microbiomes · 2023Article
- Defects in DNA double-strand break repair resensitize antibiotic-resistant Escherichia coli to multiple bactericidal antibiotics.MicrobiologyOpen · 2022Article
- Microfluidic chip-based long-term preservation and culture of engineering bacteria for DNA damage evaluation.Applied microbiology and biotechnology · 2022Article
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- Reduced Mutation Rate and Increased Transformability of Transposon-Free Acinetobacter baylyi ADP1-ISx.Applied and environmental microbiology · 2017Article
- Mutations that Separate the Functions of the Proofreading Subunit of the Escherichia coli Replicase.G3 (Bethesda, Md.) · 2015Article
- DNA Topoisomerases.EcoSal Plus · 2015Review
- Analysis of RuvABC and RecG involvement in the escherichia coli response to the covalent topoisomerase-DNA complex.Journal of bacteriology · 2010Article
- SOS response induces persistence to fluoroquinolones in Escherichia coli.PLoS genetics · 2009Article
- Hydroxyl radicals are involved in cell killing by the bacterial topoisomerase I cleavage complex.Journal of bacteriology · 2009Article
- Rapid assessment of the effect of ciprofloxacin on chromosomal DNA from Escherichia coli using an in situ DNA fragmentation assay.BMC microbiology · 2009Article
- Bacterial topoisomerase I as a target for discovery of antibacterial compounds.Nucleic acids research · 2009Review
- The epsilon subunit of DNA polymerase III Is involved in the nalidixic acid-induced SOS response in Escherichia coli.Journal of bacteriology · 2008Article
- SOS induction by stabilized topoisomerase IA cleavage complex occurs via the RecBCD pathway.Journal of bacteriology · 2008Article
- Quinolone-mediated bacterial death.Antimicrobial agents and chemotherapy · 2008Review
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 1 country.
Funding
Abstract
Nalidixic acid, the prototype antibacterial quinolone, induces the SOS response by a mechanism that requires the RecBCD nuclease/helicase. A key step inferred for this induction pathway is the conversion of a drug-induced gyrase cleavage complex into a DNA break that can be processed by RecBC. We tried to clarify the nature of this step by searching for additional gene products that are specifically necessary for SOS induction following nalidixic acid treatment. A transposon library of approximately 19,000 insertion mutants yielded 18 mutants that were substantially reduced for SOS induction following nalidixic acid but not UV treatment, and which were also hypersensitive to nalidixic acid. All 18 mutants turned out to have insertions in recB or recC. As expected, recA insertion mutants were uncovered as being uninducible by either nalidixic acid or UV treatment. Insertions in 11 other genes were found to cause partial defects in SOS induction by one or both pathways, providing possible leads in understanding the detailed mechanisms of SOS induction. Overall, these results suggest that nalidixic acid-induced DNA breaks are generated either by RecBC itself, by redundant activities, and/or by an essential protein that could not be uncovered with transposon mutagenesis.
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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.