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Chem Biol. 2014 May 22;21(5):657-65. doi: 10.1016/j.chembiol.2014.02.018. Epub 2014 Apr 10.

Synthetic interaction between the TipN polarity factor and an AcrAB-family efflux pump implicates cell polarity in bacterial drug resistance.

Author information

1
Department of Microbiology & Molecular Medicine, Institute of Genetics & Genomics in Geneva (iGE3), Faculty of Medicine/CMU, University of Geneva, Rue Michel Servet 1, 1211 Genève 4, Switzerland.
2
Department of Microbiology & Molecular Medicine, Institute of Genetics & Genomics in Geneva (iGE3), Faculty of Medicine/CMU, University of Geneva, Rue Michel Servet 1, 1211 Genève 4, Switzerland. Electronic address: patrick.viollier@unige.ch.

Abstract

Quinolone antibiotics are clinically important drugs that target bacterial DNA replication and chromosome segregation. Although the AcrAB-family efflux pumps generally protect bacteria from such drugs, the physiological role of these efflux systems and their interplay with other cellular events are poorly explored. Here, we report an intricate relationship between antibiotic resistance and cell polarity in the model bacterium Caulobacter crescentus. We show that a polarity landmark protein, TipN, identified by virtue of its ability to direct flagellum placement to the new cell pole, protects cells from toxic misregulation of an AcrAB efflux pump through a cis-encoded nalidixic acid-responsive transcriptional repressor. Alongside the importance of polarity in promoting the inheritance and activity of virulence functions including motility, we can now ascribe to it an additional role in drug resistance that is distinct from classical efflux mechanisms.

PMID:
24726830
DOI:
10.1016/j.chembiol.2014.02.018
[Indexed for MEDLINE]
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