The SOS response promotes qnrB quinolone-resistance determinant expression

Sandra Da Re; Fabien Garnier; Emilie Guérin; Susana Campoy; François Denis; Marie Cécile Ploy

doi:https://doi.org/10.1038/embor.2009.99

The SOS response promotes qnrB quinolone-resistance determinant expression

Sandra Da Re, Fabien Garnier, Emilie Guérin, Susana Campoy, François Denis, Marie Cécile Ploy

Department of Genetics and Microbiology

Research output: Contribution to journal › Article › Research › peer-review

71 Citations (Scopus)

Abstract

The qnr genes are plasmid-borne fluoroquinolone-resistance determinants widespread in Enterobacteriaceae. Three families of qnr determinants (qnrA, B and S) have been described, but little is known about their expression and regulation. Two new determinants, qnrC and qnrD, have been found recently. Here, we describe the characterization of the qnrB2 promoter and the identification of a LexA-binding site in the promoter region of all qnrB alleles. LexA is the central regulator of the SOS response to DNA damage. We show that qnrB2 expression is regulated through the SOS response in a LexA/RecA-dependent manner, and that it can be induced by the quinolone ciprofloxacin, a known inducer of the SOS system. This is the first description of direct SOS-dependent regulation of an antibiotic-resistance mechanism in response to the antibiotic itself.

Original language	English
Pages (from-to)	929-933
Journal	EMBO Reports
Volume	10
DOIs	https://doi.org/10.1038/embor.2009.99
Publication status	Published - 29 Jun 2009

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title = "The SOS response promotes qnrB quinolone-resistance determinant expression",

abstract = "The qnr genes are plasmid-borne fluoroquinolone-resistance determinants widespread in Enterobacteriaceae. Three families of qnr determinants (qnrA, B and S) have been described, but little is known about their expression and regulation. Two new determinants, qnrC and qnrD, have been found recently. Here, we describe the characterization of the qnrB2 promoter and the identification of a LexA-binding site in the promoter region of all qnrB alleles. LexA is the central regulator of the SOS response to DNA damage. We show that qnrB2 expression is regulated through the SOS response in a LexA/RecA-dependent manner, and that it can be induced by the quinolone ciprofloxacin, a known inducer of the SOS system. This is the first description of direct SOS-dependent regulation of an antibiotic-resistance mechanism in response to the antibiotic itself.",

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T1 - The SOS response promotes qnrB quinolone-resistance determinant expression

AU - Da Re, Sandra

AU - Garnier, Fabien

AU - Guérin, Emilie

AU - Campoy, Susana

AU - Denis, François

AU - Ploy, Marie Cécile

PY - 2009/6/29

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N2 - The qnr genes are plasmid-borne fluoroquinolone-resistance determinants widespread in Enterobacteriaceae. Three families of qnr determinants (qnrA, B and S) have been described, but little is known about their expression and regulation. Two new determinants, qnrC and qnrD, have been found recently. Here, we describe the characterization of the qnrB2 promoter and the identification of a LexA-binding site in the promoter region of all qnrB alleles. LexA is the central regulator of the SOS response to DNA damage. We show that qnrB2 expression is regulated through the SOS response in a LexA/RecA-dependent manner, and that it can be induced by the quinolone ciprofloxacin, a known inducer of the SOS system. This is the first description of direct SOS-dependent regulation of an antibiotic-resistance mechanism in response to the antibiotic itself.

AB - The qnr genes are plasmid-borne fluoroquinolone-resistance determinants widespread in Enterobacteriaceae. Three families of qnr determinants (qnrA, B and S) have been described, but little is known about their expression and regulation. Two new determinants, qnrC and qnrD, have been found recently. Here, we describe the characterization of the qnrB2 promoter and the identification of a LexA-binding site in the promoter region of all qnrB alleles. LexA is the central regulator of the SOS response to DNA damage. We show that qnrB2 expression is regulated through the SOS response in a LexA/RecA-dependent manner, and that it can be induced by the quinolone ciprofloxacin, a known inducer of the SOS system. This is the first description of direct SOS-dependent regulation of an antibiotic-resistance mechanism in response to the antibiotic itself.

U2 - https://doi.org/10.1038/embor.2009.99

DO - https://doi.org/10.1038/embor.2009.99

M3 - Article

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JO - EMBO Reports

JF - EMBO Reports

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The SOS response promotes qnrB quinolone-resistance determinant expression

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