recA gene expression in ciprofloxacin resistant Escherichia coli dinI- mutant

Microorganisms in response to drug development, acquire resistance through a variety of mechanisms. The prevalence of resistance to fluoroquinolones (FQ), such as ciprofluxacin in Escherichia coli has increased markedly in recent years. Mutagenesis induced by SOS catalyzes the evolution of resistance to fluoroquinolones. A member of the SOS regulon is the dinI gene. Protein encoded by the gene DinI acts as positive and negative modulator of RecA performance. Previous studies showedrecA gene expression in ciprofloxacin resistant Escherichia coli dinI in which mutants increased. The aim of this study was to investigate recA gene expression in dinI-mutant resistant to ciprofloxacin
For this purpose, dinI- mutant became ciprofloxacin resistant by encountering to increase amount of ciprofloxacin via stepwise method and be evaluated for MIC. Then, the expression of recA gene was determined in wild type, dinI- and a dinI mutants by real time PCR.
The results showed that a dinI- mutant acquired low level of resistance to ciprofloxacin and its MIC was 0.3 µg/ml. recA gene expression in the dinI- mutant was increased in comparison with wild type strain. However, the amount of increase was about one fourth of increase in dinI mutant.
Discussion and In conclusion, inactivation of dinI gene does not inhibit increase in recA gene expression and regulation of RecA activity is possibly complex and could be conducted in the absence of dinI by other regulatory proteins