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Ciprofloxacin Causes Persister Formation By Inducing The Tisb Toxin In Escherichia Coli, Tobias Dörr, Marin Vulić, Kim Lewis
Ciprofloxacin Causes Persister Formation By Inducing The Tisb Toxin In Escherichia Coli, Tobias Dörr, Marin Vulić, Kim Lewis
Marin Vulić
Bacteria induce stress responses that protect the cell from lethal factors such as DNA-damaging agents. Bacterial populations also form persisters, dormant cells that are highly tolerant to antibiotics and play an important role in recalcitrance of biofilm infections. Stress response and dormancy appear to represent alternative strategies of cell survival. The mechanism of persister formation is unknown, but isolated persisters show increased levels of toxin/antitoxin (TA) transcripts. We have found previously that one or more components of the SOS response induce persister formation after exposure to a DNA-damaging antibiotic. The SOS response induces several TA genes in Escherichia coli. Here, …
Sos Response Induces Persistence To Fluoroquinolones In Escherichia Coli, Tobias Dörr, Kim Lewis, Marin Vulić
Sos Response Induces Persistence To Fluoroquinolones In Escherichia Coli, Tobias Dörr, Kim Lewis, Marin Vulić
Marin Vulić
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 …
Ciprofloxacin Causes Persister Formation By Inducing The Tisb Toxin In Escherichia Coli, Tobias Dörr, Marin Vulić, Kim Lewis
Ciprofloxacin Causes Persister Formation By Inducing The Tisb Toxin In Escherichia Coli, Tobias Dörr, Marin Vulić, Kim Lewis
Kim Lewis
Bacteria induce stress responses that protect the cell from lethal factors such as DNA-damaging agents. Bacterial populations also form persisters, dormant cells that are highly tolerant to antibiotics and play an important role in recalcitrance of biofilm infections. Stress response and dormancy appear to represent alternative strategies of cell survival. The mechanism of persister formation is unknown, but isolated persisters show increased levels of toxin/antitoxin (TA) transcripts. We have found previously that one or more components of the SOS response induce persister formation after exposure to a DNA-damaging antibiotic. The SOS response induces several TA genes in Escherichia coli. Here, …
Persisters: A Distinct Physiological State Of E. Coli, Devang Shah, Zhigang Zhang, Arkady B. Khodursky, Niilo Kaldalu, Kristi Kurg, Kim Lewis
Persisters: A Distinct Physiological State Of E. Coli, Devang Shah, Zhigang Zhang, Arkady B. Khodursky, Niilo Kaldalu, Kristi Kurg, Kim Lewis
Kim Lewis
BackgroundBacterial populations contain persisters, phenotypic variants that constitute approximately 1% of cells in stationary phase and biofilm cultures. Multidrug tolerance of persisters is largely responsible for the inability of antibiotics to completely eradicate infections. Recent progress in understanding persisters is encouraging, but the main obstacle in understanding their nature was our inability to isolate these elusive cells from a wild-type population since their discovery in 1944. ResultsWe hypothesized that persisters are dormant cells with a low level of translation, and used this to physically sort dim E. coli cells which do not contain sufficient amounts of unstable GFP expressed from …
Sos Response Induces Persistence To Fluoroquinolones In Escherichia Coli, Tobias Dörr, Kim Lewis, Marin Vulić
Sos Response Induces Persistence To Fluoroquinolones In Escherichia Coli, Tobias Dörr, Kim Lewis, Marin Vulić
Kim Lewis
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 …