Bacteria can survive antibiotic treatment without acquiring heritable antibiotic resistance. We investigated persistence to the fluoroquinolone ciprofloxacin in Escherichia coli. Our data show that a majority of persisters to ciprofloxacin were formed upon exposure to the antibiotic, in a manner dependent on the SOS gene network. These findings reveal an active and inducible mechanism of persister formation mediated by the SOS response, challenging the prevailing view that persisters are pre-existing and formed purely by stochastic means. SOS-induced persistence is a novel mechanism by which cells can counteract DNA damage and promote survival to fluoroquinolones. This unique survival mechanism may be an important factor influencing the outcome of antibiotic therapy in vivo.
bacteria, persisters, SOS gene network, fluoroquinolones
Drug resistance in microorganisms, Antibiotics, Escherichia coli, Ciprofloxacin
Public Library of Science Genetics
Copyright 2009. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. This work was supported by an NIH grant ‘‘A genomics approach to drug tolerance’’ 3R01 GM061162-05A1. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Tobias Dörr, Kim Lewis, Marin Vulić
Dörr, Tobias; Lewis, Kim; and Vulić, Marin, "SOS response induces persistence to fluoroquinolones in Escherichia coli" (2009). Biology Faculty Publications. Paper 12. http://hdl.handle.net/2047/d20000893
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Additional FilesSOS figure 1.tif (520 kB)
SOS figure 2.tif (270 kB)
sos figure 3.tif (79 kB)
sos figure 4.tif (235 kB)
sos figure 5.tif (72 kB)
sos figure 6.tif (84 kB)
SOS table 1.tif (285 kB)