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The SOS response promotes qnrB quinolone‐resistance determinant expression
Author(s) -
Da Re Sandra,
Garnier Fabien,
Guérin Emilie,
Campoy Susana,
Denis François,
Ploy MarieCécile
Publication year - 2009
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1038/embor.2009.99
Subject(s) - repressor lexa , sos response , biology , genetics , plasmid , quinolone , gene , regulon , inducer , regulation of gene expression , dna damage , repressor , microbiology and biotechnology , dna , gene expression , antibiotics
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.