Journal
MOLECULAR CELL
Volume 59, Issue 1, Pages 9-21Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2015.05.011
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Funding
- Fund for Scientific Research, Flanders (FWO)
- Institute for Promotion of Innovation through Science and Technology in Flanders (IWT Vlaanderen)
- KU Leuven Research Council [PF/10/010 [NATAR], IDO/07/010, IDO/09/010, CREA/08/023]
- Ghent University (Multidisciplinary Research Partnership M2N'')
- FWO [G.0299.07, G.0413.10, G.0471.12N, G0B2515N]
- Hercules Foundation [HER/08/21]
- Flemish Government
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Within bacterial populations, a small fraction of per-sister cells is transiently capable of surviving exposure to lethal doses of antibiotics. As a bet-hedging strategy, persistence levels are determined both by stochastic induction and by environmental stimuli called responsive diversification. Little is known about the mechanisms that link the low frequency of per-sisters to environmental signals. Our results support a central role for the conserved GTPase Obg in determining persistence in Escherichia coli in response to nutrient starvation. Obg-mediated persistence requires the stringent response alarmone (p) ppGpp and proceeds through transcriptional control of the hokB-sokB type I toxin-antitoxin module. In individual cells, increased Obg levels induce HokB expression, which in turn results in a collapse of the membrane potential, leading to dormancy. Obg also controls persistence in Pseudomonas aeruginosa and thus constitutes a conserved regulator of antibiotic tolerance. Combined, our findings signify an important step toward unraveling shared genetic mechanisms underlying persistence.
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