ArticleThe Journal of antimicrobial chemotherapy2011
Topoisomerase I function during Escherichia coli response to antibiotics and stress enhances cell killing from stabilization of its cleavage complex.
Article in The Journal of antimicrobial chemotherapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Microgravity reshapes bacteriophage-host coevolution aboard the International Space Station.PLoS biology · 2026Article
- Combination of bactericidal antibiotics and inhibitors of Universal stress protein A (UspA): a potential therapeutic alternative against multidrug resistant Escherichia coli in urinary tract infections.The Journal of antibiotics · 2022Article
- Crystal structure of the 65-kilodalton amino-terminal fragment of DNA topoisomerase I from the gram-positive model organism Streptococcus mutans.Biochemical and biophysical research communications · 2019Article
- The Role ofFrontiers in cellular and infection microbiology · 2019Article
- Comparative proteomic analysis of Neisseria meningitidis wildtype and dprA null mutant strains links DNA processing to pilus biogenesis.BMC microbiology · 2017Article
- Article
- A simplified protocol for high-yield expression and purification of bacterial topoisomerase I.Protein expression and purification · 2016Article
- Article
- Targeting bacterial topoisomerase I to meet the challenge of finding new antibiotics.Future medicinal chemistry · 2015Review
- 3,4-dimethoxyphenyl bis-benzimidazole, a novel DNA topoisomerase inhibitor that preferentially targets Escherichia coli topoisomerase I.The Journal of antimicrobial chemotherapy · 2012Article
- Engineering Escherichia coli to increase plasmid DNA production in high cell-density cultivations in batch mode.Microbial cell factories · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectivesTo explore the role of topoisomerase I in gene activation and increased RecA levels during the bacterial SOS response, as well as the effect of antibiotic treatment and stress challenge on cell killing initiated by trapped topoisomerase I cleavage complex.
methodsA mutant Escherichia coli strain with a ΔtopA mutation was used to investigate the role of topoisomerase I function in the SOS response to trimethoprim and mitomycin C. Induction of the recA and dinD1 promoters was measured using luciferase reporters of these promoters fused to luxCDABE. An increase in the RecA level following trimethoprim treatment was quantified directly by western blotting. The effect of stress challenge from trimethoprim and acidified nitrite treatments on cell killing by topoisomerase I cleavage complex accumulation was measured by the decrease in viability following induction of recombinant mutant topoisomerase I that forms a stabilized cleavage complex.
resultsTopoisomerase I function was found to be required for efficient transcriptional activation of the recA and dinD1 promoters during the E. coli SOS response to trimethoprim and mitomycin C. The role of topoisomerase I in the SOS response was confirmed with quantitative western blot analysis of RecA following trimethoprim treatment. The bactericidal effect from topoisomerase I cleavage complex accumulation was shown to be enhanced by stress challenge from trimethoprim and acidified nitrite.
conclusionsBacterial topoisomerase I function is actively involved in the SOS response to antibiotics and stress challenge. Cell killing initiated by the topoisomerase I cleavage complex would be enhanced by antibiotics and the host response. These findings provide further support for bacterial topoisomerase I as a therapeutic target.
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