Transcriptomic and functional analisys of the regulation os the SOS response by ciprofloxacin in Pseudomonas aeruginosa

Abstract

Chemical and physical agents may induce genetic variation in bacterial populations. The constant exposure to low concentrations of antibiotics is an important factor in the selection of strains resistant to antibacterials. In addition, some antibiotics are capable of inducing genetic variation through the generation of DNA damage, which activate an emergency response, the SOS response. This system is regulated by LexA autolysis after binding of RecA to single strands of damaged DNA during replication fork blockage. The SOS system promotes an increased rate of homologous recombination, expression of error-prone DNA polymerases, inhibition of cell division, among others. Ciprofloxacin is a potent inducer of SOS response, thus, a mutagenicity mediated by exposure to this antibiotic may be observed. Ciprofloxacin is widely used in Pseudomonas aeruginosa infection treatments. Important questions about the regulation of the SOS system by ciprofloxacin have not yet been elucidated. Previous studies have shown that the antibiotic amikacin suppresses the activation of the SOS system mediated by RecA protein during treatment with ciprofloxacin in P. aeruginosa. In this work, we intend to understand the general regulation of the SOS response by ciprofloxacin and the suppression of recA by amikacin through transcriptomic analysis. We also aim to investigate the general regulation aspects of specific SOS response gene. (AU)