Journal
NATURE COMMUNICATIONS
Volume 4, Issue -, Pages -Publisher
NATURE RESEARCH
DOI: 10.1038/ncomms2607
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Funding
- French Ministry of Science and Education
- Institut Pasteur, Centre National de la Recherche Scientifique [CNRS-UMR 3525]
- French National Research Agency [ANR-08-MIE-016]
- LABEX IBEID
- European Union Seventh Framework Programme EvoTAR
- DIM Malinf
- Ministerio de Ciencia e Innovacion, Instituto de Salud Carlos III [PI10/00105, REIPI (RD06/0008)]
- [FP7-HEALTH-F3-2010-241476]
- [ANR-09-BLAN-0251]
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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 beta-lactam antibiotics cause reactive oxygen species production and induce PolIV-dependent mutagenesis in Escherichia coli. Here we show that subinhibitory concentrations of beta-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.
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