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Obg and membrane depolarization are part of a microbial bet-hedging strategy that leads to antibiotic tolerance

Natalie Verstraeten, Wouter Joris Knapen, Cyrielle Ines Kint, Veerle Liebens, Bram Van den Bergh, Liselot Dewachter, Joran Elie Michiels, Qiang Fu, Charlotte Claudia David, Ana Carolina Fierro, et al.
(2015) MOLECULAR CELL. 59(1). p.9-21
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Abstract
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.
Keywords
PSEUDOMONAS-AERUGINOSA, BACTERIAL PERSISTENCE, ESCHERICHIA-COLI K-12, GTP-BINDING PROTEIN, STRINGENT RESPONSE, PHENOTYPIC VARIABILITY, CELLS, (P)PPGPP, CHROMOSOME, STRESS

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MLA
Verstraeten, Natalie, et al. “Obg and Membrane Depolarization Are Part of a Microbial Bet-Hedging Strategy That Leads to Antibiotic Tolerance.” MOLECULAR CELL, vol. 59, no. 1, 2015, pp. 9–21, doi:10.1016/j.molcel.2015.05.011.
APA
Verstraeten, N., Knapen, W. J., Kint, C. I., Liebens, V., Van den Bergh, B., Dewachter, L., … Michiels, J. (2015). Obg and membrane depolarization are part of a microbial bet-hedging strategy that leads to antibiotic tolerance. MOLECULAR CELL, 59(1), 9–21. https://doi.org/10.1016/j.molcel.2015.05.011
Chicago author-date
Verstraeten, Natalie, Wouter Joris Knapen, Cyrielle Ines Kint, Veerle Liebens, Bram Van den Bergh, Liselot Dewachter, Joran Elie Michiels, et al. 2015. “Obg and Membrane Depolarization Are Part of a Microbial Bet-Hedging Strategy That Leads to Antibiotic Tolerance.” MOLECULAR CELL 59 (1): 9–21. https://doi.org/10.1016/j.molcel.2015.05.011.
Chicago author-date (all authors)
Verstraeten, Natalie, Wouter Joris Knapen, Cyrielle Ines Kint, Veerle Liebens, Bram Van den Bergh, Liselot Dewachter, Joran Elie Michiels, Qiang Fu, Charlotte Claudia David, Ana Carolina Fierro, Kathleen Marchal, Jan Beirlant, Wim Versées, Johan Hofkens, Maarten Jansen, Maarten Fauvart, and Jan Michiels. 2015. “Obg and Membrane Depolarization Are Part of a Microbial Bet-Hedging Strategy That Leads to Antibiotic Tolerance.” MOLECULAR CELL 59 (1): 9–21. doi:10.1016/j.molcel.2015.05.011.
Vancouver
1.
Verstraeten N, Knapen WJ, Kint CI, Liebens V, Van den Bergh B, Dewachter L, et al. Obg and membrane depolarization are part of a microbial bet-hedging strategy that leads to antibiotic tolerance. MOLECULAR CELL. 2015;59(1):9–21.
IEEE
[1]
N. Verstraeten et al., “Obg and membrane depolarization are part of a microbial bet-hedging strategy that leads to antibiotic tolerance,” MOLECULAR CELL, vol. 59, no. 1, pp. 9–21, 2015.
@article{7026829,
  abstract     = {{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.}},
  author       = {{Verstraeten, Natalie and Knapen, Wouter Joris and Kint, Cyrielle Ines and Liebens, Veerle and Van den Bergh, Bram and Dewachter, Liselot and Michiels, Joran Elie and Fu, Qiang and David, Charlotte Claudia and Fierro, Ana Carolina and Marchal, Kathleen and Beirlant, Jan and Versées, Wim and Hofkens, Johan and Jansen, Maarten and Fauvart, Maarten and Michiels, Jan}},
  issn         = {{1097-2765}},
  journal      = {{MOLECULAR CELL}},
  keywords     = {{PSEUDOMONAS-AERUGINOSA,BACTERIAL PERSISTENCE,ESCHERICHIA-COLI K-12,GTP-BINDING PROTEIN,STRINGENT RESPONSE,PHENOTYPIC VARIABILITY,CELLS,(P)PPGPP,CHROMOSOME,STRESS}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{9--21}},
  title        = {{Obg and membrane depolarization are part of a microbial bet-hedging strategy that leads to antibiotic tolerance}},
  url          = {{http://doi.org/10.1016/j.molcel.2015.05.011}},
  volume       = {{59}},
  year         = {{2015}},
}
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