DinI could be a suitable option in drug targeting strategies to reduce SOS mutagenesis

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Pourahmad Jaktaji Razieh; Mohammadi Sare

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Journal Paper

Paper Information

Journal: JOURNAL OF MICROBIAL BIOLOGY Year:2025 | Volume:14 | Issue:55 Page(s): 1-6

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Title

DinI could be a suitable option in drug targeting strategies to reduce SOS mutagenesis

Author(s)

Pourahmad Jaktaji Razieh | Mohammadi Sare | Issue Writer Certificate

Keywords

Ciprofloxacin

DinI

Escherichia coli

Mutagenesis

SOS response

Abstract

Ciprofloxacin induces the SOS response. Induction of the SOS response confers resistance to ciprofloxacin through activation of DNA polymerase V. However, mutations in lexA, umuDC and especially recA prevent the evolution of resistance to ciprofloxacin. Alternatively, mutations in SOS proteins that regulate RecA activity, such as DinI, can reduce SOS mutagenesis. The aim of this study was to investigate the effect of DinI inactivation on the frequency of mutagenesis and expression of the umuD and rdgC genes after treatment with ciprofloxacin and to examine the promoter region and the 3′ end of the recA gene for possible changes in dinI (SM1 and SM2) mutants. Ciprofloxacin-resistant clones (SM1 and SM2) derived from the JW10481 (dinI- ) strain were used in this study. Mutagenesis analysis and real-time PCR were used to measure the frequency of mutant cells and the expression of umuD and rdgC genes in mutants, respectively. The promoter region and recA gene sequence were examined by PCR amplification and DNA sequencing in dinI- clones. SOS mutagenesis was significantly reduced (P<0.05) in SM1 and SM2 clones. These clones (dinI-) did not show overexpression of the umuD gene. rdgC gene was overexpressed in SM2, but not in the M2 mutant with intact dinI gene. Furthermore, DNA sequencing did not reveal any change in the recA gene sequence. The low frequency of mutagenesis and umuD expression in clones lacking DinI protein activity demonstrated the importance of this protein in SOS mutagenesis. In conclusion, DinI may be a suitable option in drug targeting strategies to enhance the efficacy of ciprofloxacin in combination therapy against a variety of infections caused by Escherichia coli and other Gram-negative bacteria with homologues of this protein.

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