Inactivation of UmuC Protein Significantly Reduces Resistance to Ciprofloxacin and SOS Mutagenesis in Escherichia coli Mutants Harboring Intact umuD Gene

نویسندگان

چکیده

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

برای دانلود باید عضویت طلایی داشته باشید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Regulation of SOS mutagenesis by proteolysis ( UmuD / D ' / UmuC / Lon / ClpXP / protein - protein interactions )

DNA damage-inducible mutagenesis in Escherichia coli is largely dependent upon the activity of the UmuD (UmuD') and UmuC proteins. The intracellular level of these proteins is tightly regulated at both the transcriptional and the posttranslational levels. Such regulation presumably allows cells to deal with DNA damage via error-free repair pathways before being committed to error-prone pathways...

متن کامل

RecA protein-dependent cleavage of UmuD protein and SOS mutagenesis.

Induction of the Escherichia coli SOS system increases the ability of the cell to perform DNA repair and mutagenesis. Products of the recA and umuD,C genes are required for mutagenesis induced by radiation and many chemicals. Transcription of the SOS genes including recA and umuD,C is repressed by a repressor, LexA protein, and is derepressed by the proteolytic cleavage of LexA facilitated by R...

متن کامل

Dual role for Escherichia coli RecA protein in SOS mutagenesis.

Induction of the Escherichia coli SOS system increases the ability of the cells to perform DNA repair and mutagenesis. Previous work has shown that this increased mutagenesis is the result of derepression of specific genes through a complex regulatory mechanism controlled by LexA and RecA proteins. One role of RecA protein in this process is to facilitate proteolytic cleavage of LexA protein (t...

متن کامل

Regulation of E . coli SOS Mutagenesis by Dimeric Intrinsically Disordered umuD Gene Products

Products of the umuD gene in E. coli are involved in regulating the timing of error-free DNA repair processes and mutagenic translesion DNA synthesis (TLS) during the SOS response to DNA damage. Homodimeric UmuD2 is upregulated early during the SOS response, and a slow post-translational autocleavage process removes the N-terminal 24 amino acids of each UmuD monomer. The remaining C-terminal fr...

متن کامل

Study the Expression of marA Gene in Ciprofloxacin and Tetracycline Resistant Mutants of Esherichia coli

MarA activates two membrane dependent mechanisms of resistance to different antibiotics, such as ciprofloxacin and tetracycline, including promotion of outflux and inhibition of influx of antibiotics. Thus, MarA causes multiple antibiotic resistance phenotype. The activation of these mechanisms needs overexpression of marA. This could happen through mutation in marR. Thus, the aim of this study...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

ژورنال

عنوان ژورنال: Jundishapur Journal of Microbiology

سال: 2021

ISSN: ['2008-3645', '2008-4161']

DOI: https://doi.org/10.5812/jjm.111828