{"id":6464,"date":"2022-01-17T13:21:00","date_gmt":"2022-01-17T12:21:00","guid":{"rendered":"https:\/\/fhu-premimpact.org\/?post_type=publication&#038;p=6464"},"modified":"2023-02-09T13:24:54","modified_gmt":"2023-02-09T12:24:54","slug":"a-qnr-plasmid-allows-aminoglycosides-to-induce-sos-in-escherichia-coli","status":"publish","type":"publication","link":"https:\/\/fhu-premimpact.org\/en\/publications\/a-qnr-plasmid-allows-aminoglycosides-to-induce-sos-in-escherichia-coli\/","title":{"rendered":"<a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/35037621\/\">A <em>qnr<\/em>-plasmid allows aminoglycosides to induce SOS in <em>Escherichia coli<\/em>.<\/a>"},"content":{"rendered":"\n<h2 class=\"wp-block-heading\">Abstract<\/h2>\n\n\n\n<p>The plasmid-mediated quinolone resistance (PMQR) genes have been shown to promote high-level bacterial resistance to fluoroquinolone antibiotics, potentially leading to clinical treatment failures. In <em>Escherichia coli<\/em>, sub-minimum inhibitory concentrations (sub-MICs) of the widely used fluoroquinolones are known to induce the SOS response. Interestingly, the expression of several PMQR <em>qnr<\/em> genes is controlled by the SOS master regulator, LexA. During the characterization of a small <em>qnrD<\/em>-plasmid carried in <em>E. coli,<\/em> we observed that the aminoglycosides become able to induce the SOS response in this species, thus leading to the elevated transcription of <em>qnrD<\/em>. Our findings show that the induction of the SOS response is due to nitric oxide (NO) accumulation in the presence of sub-MIC of aminoglycosides. We demonstrated that the NO accumulation is driven by two plasmid genes, ORF3 and ORF4, whose products act at two levels. ORF3 encodes a putative flavin adenine dinucleotide (<em>FAD<\/em>)-binding oxidoreductase which helps NO synthesis, while ORF4 codes for a putative fumarate and nitrate reductase (<em>FNR<\/em>)-type transcription factor, related to an O<sub>2<\/sub>-responsive regulator of <em>hmp<\/em> expression, able to repress the Hmp-mediated NO detoxification pathway of <em>E. coli<\/em>. Thus, this discovery, that other major classes of antibiotics may induce the SOS response could have worthwhile implications for antibiotic stewardship efforts in preventing the emergence of resistance.<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Elife. 2022 Jan 17;11:e69511. doi: 10.7554\/eLife.69511.<\/p>\n","protected":false},"featured_media":0,"template":"","class_list":["post-6464","publication","type-publication","status-publish","hentry"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.2 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>A qnr-plasmid allows aminoglycosides to induce SOS in Escherichia coli. - FHU Prem&#039;IMPACT<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/fhu-premimpact.org\/en\/publications\/a-qnr-plasmid-allows-aminoglycosides-to-induce-sos-in-escherichia-coli\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"A qnr-plasmid allows aminoglycosides to induce SOS in Escherichia coli. - 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