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Involvement of toxin-antitoxin modules in Burkholderia cenocepacia biofilm persistence

Heleen Van Acker (UGent) , Andrea Sass (UGent) , Inne Dhondt (UGent) , Hans Nelis (UGent) and Tom Coenye (UGent)
(2014) PATHOGENS AND DISEASE. 71(3). p.326-335
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Abstract
Biofilms are involved in the recalcitrance of infections due to the presence of persister cells. Although the molecular basis of persistence is still largely unknown, toxin-antitoxin modules (TA) are thought to play a role in this process. In this study, we investigated whether TA modules contribute to persistence toward antibiotics in Burkholderia cenocepacia J2315. Sixteen pairs of genes were identified based on their apparent similarity to TA modules. Overexpression of the putative toxins had various effects on growth, persistence, and biofilm formation. Toxins, whose overexpression resulted in growth inhibition, often increased the number of surviving persisters; in contrast, overexpression of putative toxins showing no effects on growth had no positive influence on the number of surviving persisters. Furthermore, the expression of the TA modules was compared between treated and untreated sessile and planktonic wild-type cultures. For 10 toxin-encoding genes, the expression was higher in untreated sessile cells than in untreated planktonic cells. Nine toxin-encoding genes were upregulated after treatment with tobramycin, but none after treatment with ciprofloxacin. These results indicate that most, but not all TA modules contribute to persistence in B. cenocepacia J2315 and that this contribution depends on the mode of growth and the antibiotic used.
Keywords
persistence, biofilm, burkholderia, toxin antitoxin module, ESCHERICHIA-COLI, BACTERIAL PERSISTENCE, SYSTEMS, PLASMID, CELLS, LOCI

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MLA
Van Acker, Heleen, Andrea Sass, Inne Dhondt, et al. “Involvement of Toxin-antitoxin Modules in Burkholderia Cenocepacia Biofilm Persistence.” PATHOGENS AND DISEASE 71.3 (2014): 326–335. Print.
APA
Van Acker, Heleen, Sass, A., Dhondt, I., Nelis, H., & Coenye, T. (2014). Involvement of toxin-antitoxin modules in Burkholderia cenocepacia biofilm persistence. PATHOGENS AND DISEASE, 71(3), 326–335.
Chicago author-date
Van Acker, Heleen, Andrea Sass, Inne Dhondt, Hans Nelis, and Tom Coenye. 2014. “Involvement of Toxin-antitoxin Modules in Burkholderia Cenocepacia Biofilm Persistence.” Pathogens and Disease 71 (3): 326–335.
Chicago author-date (all authors)
Van Acker, Heleen, Andrea Sass, Inne Dhondt, Hans Nelis, and Tom Coenye. 2014. “Involvement of Toxin-antitoxin Modules in Burkholderia Cenocepacia Biofilm Persistence.” Pathogens and Disease 71 (3): 326–335.
Vancouver
1.
Van Acker H, Sass A, Dhondt I, Nelis H, Coenye T. Involvement of toxin-antitoxin modules in Burkholderia cenocepacia biofilm persistence. PATHOGENS AND DISEASE. 2014;71(3):326–35.
IEEE
[1]
H. Van Acker, A. Sass, I. Dhondt, H. Nelis, and T. Coenye, “Involvement of toxin-antitoxin modules in Burkholderia cenocepacia biofilm persistence,” PATHOGENS AND DISEASE, vol. 71, no. 3, pp. 326–335, 2014.
@article{5645124,
  abstract     = {{Biofilms are involved in the recalcitrance of infections due to the presence of persister cells. Although the molecular basis of persistence is still largely unknown, toxin-antitoxin modules (TA) are thought to play a role in this process. In this study, we investigated whether TA modules contribute to persistence toward antibiotics in Burkholderia cenocepacia J2315. Sixteen pairs of genes were identified based on their apparent similarity to TA modules. Overexpression of the putative toxins had various effects on growth, persistence, and biofilm formation. Toxins, whose overexpression resulted in growth inhibition, often increased the number of surviving persisters; in contrast, overexpression of putative toxins showing no effects on growth had no positive influence on the number of surviving persisters. Furthermore, the expression of the TA modules was compared between treated and untreated sessile and planktonic wild-type cultures. For 10 toxin-encoding genes, the expression was higher in untreated sessile cells than in untreated planktonic cells. Nine toxin-encoding genes were upregulated after treatment with tobramycin, but none after treatment with ciprofloxacin. These results indicate that most, but not all TA modules contribute to persistence in B. cenocepacia J2315 and that this contribution depends on the mode of growth and the antibiotic used.}},
  author       = {{Van Acker, Heleen and Sass, Andrea and Dhondt, Inne and Nelis, Hans and Coenye, Tom}},
  issn         = {{2049-632X}},
  journal      = {{PATHOGENS AND DISEASE}},
  keywords     = {{persistence,biofilm,burkholderia,toxin antitoxin module,ESCHERICHIA-COLI,BACTERIAL PERSISTENCE,SYSTEMS,PLASMID,CELLS,LOCI}},
  language     = {{eng}},
  number       = {{3}},
  pages        = {{326--335}},
  title        = {{Involvement of toxin-antitoxin modules in Burkholderia cenocepacia biofilm persistence}},
  url          = {{http://dx.doi.org/10.1111/2049-632X.12177}},
  volume       = {{71}},
  year         = {{2014}},
}

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