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Volume 10Nov 2009

Scientific Report

  • EMBO reports (2009) 10, 929 - 933
  • doi:10.1038/embor.2009.99

Published online: 26 June 2009

The SOS response promotes qnrB quinolone-resistance determinant expression

Sandra Da Re1,2, Fabien Garnier1,3, Emilie Guérin1,2, Susana Campoy4, François Denis1,2,3 & Marie-Cécile Ploy1,2,3

  1. INSERM, Equipe Avenir, and
  2. Université de Limoges, Faculté de Médecine, EA3175, 2 Rue du Docteur Marcland, 87025 Limoges Cedex, France
  3. CHU Limoges, Laboratoire de Bactériologie-Virologie-Hygiène, 2 Avenue Martin Luther King, 87042 Limoges Cedex, France
  4. Departament de Genètica i Microbiologia, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain

Correspondence to:

Marie-Cécile Ploy, Tel: +33 5 55 05 67 27; Fax: +33 5 55 05 67 22;
E-mail: marie-cecile.ploy@unilim.fr

Received 23 October 2008; Revised 20 March 2009; Accepted 9 April 2009

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.

  • Keywords:

    • antibiotic resistance,
    • ciprofloxacin,
    • qnrB,
    • SOS response