Plasmid pSK 1002-mediated mutator effect and SOS response and SOS mutagenesis of 2,5-dichloronitrobenzol in Salmonella typhimurium

1991 ◽  
Vol 264 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Zhong-chu Jin ◽  
Jing Qian
Keyword(s):  
Salmonella Typhimurium ◽  
Sos Response ◽  
Sos Mutagenesis ◽  
Mutator Effect

Mutagenesis and More: umuDC and the Escherichia coli SOS Response

Genetics ◽  
1998 ◽  
Vol 148 (4) ◽  
pp. 1599-1610 ◽  
Author(s):  
Bradley T Smith ◽  
Graham C Walker
Keyword(s):  
Escherichia Coli ◽  
Dna Damage ◽  
Cellular Response ◽  
Sos Response ◽  
Posttranslational Regulation ◽  
E Coli ◽  
Sos Mutagenesis ◽  
Induced Mutagenesis ◽  
Mechanistic Basis ◽  
Increase Cell Survival

Abstract The cellular response to DNA damage that has been most extensively studied is the SOS response of Escherichia coli. Analyses of the SOS response have led to new insights into the transcriptional and posttranslational regulation of processes that increase cell survival after DNA damage as well as insights into DNA-damage-induced mutagenesis, i.e., SOS mutagenesis. SOS mutagenesis requires the recA and umuDC gene products and has as its mechanistic basis the alteration of DNA polymerase III such that it becomes capable of replicating DNA containing miscoding and noncoding lesions. Ongoing investigations of the mechanisms underlying SOS mutagenesis, as well as recent observations suggesting that the umuDC operon may have a role in the regulation of the E. coli cell cycle after DNA damage has occurred, are discussed.

scholarly journals Suppression of Mutagens-Induced SOS Response by Phytoncide Solution Using Salmonella typhimurium TA1535/pSK1002 umu Test

2008 ◽  
Vol 57 (7) ◽  
pp. 381-390 ◽  
Author(s):  
Masayoshi Hisama ◽  
Sanae Matsuda ◽  
Tomomi Tanaka ◽  
Hiroharu Shibayama ◽  
Masato Nomura ◽  
...  
Keyword(s):  
Salmonella Typhimurium ◽  
Sos Response

scholarly journals Inactivation of Umuc Protein Significantly Reduces Resistance to Ciprofloxacin and SOS Mutagenesis in Escherichia coli Mutants Harboring Intact Umud Gene

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Razieh Pourahmad Jaktaji ◽  
Sayedeh Marzieh Nourbakhsh Rezaei
Keyword(s):  
Escherichia Coli ◽  
Dna Polymerase ◽  
Genetic Background ◽  
Pcr Amplification ◽  
Sos Response ◽  
Rpob Gene ◽  
Dilution Method ◽  
E Coli ◽  
Sos Mutagenesis ◽  
Dna Polymerase V

Background: Ciprofloxacin induces SOS response and mutagenesis by activation of UmuD’2C (DNA polymerase V) and DinB (DNA polymerase IV) in Escherichia coli, leading to antibiotic resistance during therapy. Inactivation of DNA polymerase V can result in the inhibition of mutagenesis in E. coli. Objectives: The aim of this research was to investigate the effect of UmuC inactivation on resistance to ciprofloxacin and SOS mutagenesis in E. coli mutants. Methods: Ciprofloxacin-resistant mutants were produced in a umuC- genetic background in the presence of increasing concentrations of ciprofloxacin. The minimum inhibitory concentration of umuC-mutants was measured by broth dilution method. Alterations in the rifampin resistance-determing region of rpoB gene were assessed by PCR amplification and DNA sequencing. The expression of SOS genes was measured by quantitative real-time PCR assay. Results: Results showed that despite the induction of SOS response (overexpression of recA, dinB, and umuD genes) following exposure to ciprofloxacin in E. coliumuC mutants, resistance to ciprofloxacin and SOS mutagenesis significantly decreased. However, rifampicin-resistant clones emerged in this genetic background. One of these clones showed mutations in the rifampicin resistance-determining region of rpoB (cluster II). The low mutation frequency of E. coli might be associated with the presence and overexpression of umuD gene, which could somehow limit the activity of DinB, the location and type of mutations in the β subunit of RNA polymerase. Conclusions: In conclusion, for increasing the efficiency of ciprofloxacin against Gram-negative bacteria, use of an inhibitor of umuC, along with ciprofloxacin, would be helpful.

scholarly journals Suppressive Effects of the Extract from Sake Cake on Chemical Mutagen-Induced SOS Response in Salmonella typhimurium.

2001 ◽  
Vol 7 (1) ◽  
pp. 64-66
Author(s):  
Yuka ISOBE ◽  
Tomoyo KATAMOTO ◽  
Yuki KAWAGUCHI ◽  
Sachiko MATSUSHITA ◽  
Kumio YOKOIGAWA ◽  
...  
Keyword(s):  
Salmonella Typhimurium ◽  
Sos Response ◽  
Chemical Mutagen

N-acetylcysteine blocks SOS induction and mutagenesis produced by fluoroquinolones in Escherichia coli

2019 ◽  
Vol 74 (8) ◽  
pp. 2188-2196 ◽  
Author(s):  
Ana I Rodríguez-Rosado ◽  
Estela Ynés Valencia ◽  
Alexandro Rodríguez-Rojas ◽  
Coloma Costas ◽  
Rodrigo S Galhardo ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Sos Response ◽  
Mutagenic Effect ◽  
Coli Strain ◽  
New Drugs ◽  
Ros Production ◽  
Sos Mutagenesis ◽  
Sos Induction ◽  
Key Factor ◽  
Bacterial Mutagenesis

AbstractBackgroundFluoroquinolones such as ciprofloxacin induce the mutagenic SOS response and increase the levels of intracellular reactive oxygen species (ROS). Both the SOS response and ROS increase bacterial mutagenesis, fuelling the emergence of resistant mutants during antibiotic treatment. Recently, there has been growing interest in developing new drugs able to diminish the mutagenic effect of antibiotics by modulating ROS production and the SOS response.ObjectivesTo test whether physiological concentrations of N-acetylcysteine, a clinically safe antioxidant drug currently used in human therapy, is able to reduce ROS production, SOS induction and mutagenesis in ciprofloxacin-treated bacteria without affecting antibiotic activity.MethodsThe Escherichia coli strain IBDS1 and its isogenic mutant deprived of SOS mutagenesis (TLS−) were treated with different concentrations of ciprofloxacin, N-acetylcysteine or both drugs in combination. Relevant parameters such as MICs, growth rates, ROS production, SOS induction, filamentation and antibiotic-induced mutation rates were evaluated.ResultsTreatment with N-acetylcysteine reduced intracellular ROS levels (by ∼40%), as well as SOS induction (by up to 75%) and bacterial filamentation caused by subinhibitory concentrations of ciprofloxacin, without affecting ciprofloxacin antibacterial activity. Remarkably, N-acetylcysteine completely abolished SOS-mediated mutagenesis.ConclusionsCollectively, our data strongly support the notion that ROS are a key factor in antibiotic-induced SOS mutagenesis and open the possibility of using N-acetylcysteine in combination with antibiotic therapy to hinder the development of antibiotic resistance.

Sign in / Sign up

Export Citation Format

Share Document