Maiques, ElisaUbeda, CarlesCampoy Sánchez, SusanaSalvador, NoeliaLasa Uzcudun, ÍñigoNovick, Richard P.Barbé, JordiPenadés, José R.2019-01-212019-01-2120060021-9193 (Print)1098-5530 (Electronic)10.1128/jb.188.7.2726-2729.2006https://academica-e.unavarra.es/handle/2454/32031Antibiotics that interfere with DNA replication and cell viability activate the SOS response. In Staphylococcus aureus, the antibiotic-induced SOS response promotes replication and high-frequency horizontal transfer of pathogenicity island-encoded virulence factors. Here we report that β-lactams induce a bona fide SOS response in S. aureus, characterized by the activation of the RecA and LexA proteins, the two master regulators of the SOS response. Moreover, we show that β-lactams are capable of triggering staphylococcal prophage induction in S. aureus lysogens. Consequently, and as previously described for SOS induction by commonly used fluoroquinolone antibiotics, β-lactam-mediated phage induction also resulted in replication and high-frequency transfer of the staphylococcal pathogenicity islands, showing that such antibiotics may have the unintended consequence of promoting the spread of bacterial virulence factors.4 p.application/pdfeng© 2006, American Society for Microbiology. All Rights Reserved.Beta-lactamsStaphylococcus aureusSOS responseHorizontal transferVirulence factorsinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccess