β-lactam antibiotics promote bacterial mutagenesis via an RpoS-mediated reduction in replication fidelity

A. Gutierrez, L. Laureti, S. Crussard, H. Abida, A. Rodríguez-Rojas, J. Blázquez, Z. Baharoglu, D. Mazel, F. Darfeuille, J. Vogel and I. Matic ()
Additional contact information
A. Gutierrez: INSERM U1001, Université Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine Paris Descartes
L. Laureti: INSERM U1001, Université Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine Paris Descartes
S. Crussard: INSERM U1001, Université Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine Paris Descartes
H. Abida: INSERM U1001, Université Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine Paris Descartes
A. Rodríguez-Rojas: Centro Nacional de Biotecnología
J. Blázquez: Centro Nacional de Biotecnología
Z. Baharoglu: Institut Pasteur, Unité Plasticité du Génome Bactérien, CNRS UMR3525
D. Mazel: Institut Pasteur, Unité Plasticité du Génome Bactérien, CNRS UMR3525
F. Darfeuille: Université Bordeaux Segalen, INSERM U869
J. Vogel: Institute for Molecular Infection Biology, University of Würzburg
I. Matic: INSERM U1001, Université Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine Paris Descartes

Nature Communications, 2013, vol. 4, issue 1, 1-9

Abstract: Abstract Regardless of their targets and modes of action, subinhibitory concentrations of antibiotics can have an impact on cell physiology and trigger a large variety of cellular responses in different bacterial species. Subinhibitory concentrations of β-lactam antibiotics cause reactive oxygen species production and induce PolIV-dependent mutagenesis in Escherichia coli. Here we show that subinhibitory concentrations of β-lactam antibiotics induce the RpoS regulon. RpoS-regulon induction is required for PolIV-dependent mutagenesis because it diminishes the control of DNA-replication fidelity by depleting MutS in E. coli, Vibrio cholerae and Pseudomonas aeruginosa. We also show that in E. coli, the reduction in mismatch-repair activity is mediated by SdsR, the RpoS-controlled small RNA. In summary, we show that mutagenesis induced by subinhibitory concentrations of antibiotics is a genetically controlled process. Because this mutagenesis can generate mutations conferring antibiotic resistance, it should be taken into consideration for the development of more efficient antimicrobial therapeutic strategies.

Date: 2013
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DOI: 10.1038/ncomms2607

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