This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Spoering, A. L.
Right arrow Articles by Lewis, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Spoering, A. L.
Right arrow Articles by Lewis, K.

 Previous Article  |  Next Article 

Journal of Bacteriology, July 2006, p. 5136-5144, Vol. 188, No. 14
0021-9193/06/$08.00+0     doi:10.1128/JB.00369-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

GlpD and PlsB Participate in Persister Cell Formation in Escherichia coli

Amy L. Spoering,{dagger} Marin Vulic, and Kim Lewis*

Department of Biology, Northeastern University, Boston, Massachusetts 02115

Received 14 March 2006/ Accepted 5 May 2006

Bacterial populations produce dormant persister cells that are resistant to killing by all antibiotics currently in use, a phenomenon known as multidrug tolerance (MDT). Persisters are phenotypic variants of the wild type and are largely responsible for MDT of biofilms and stationary populations. We recently showed that a hipBA toxin/antitoxin locus is part of the MDT mechanism in Escherichia coli. In an effort to find additional MDT genes, an E. coli expression library was selected for increased survival to ampicillin. A clone with increased persister production was isolated and was found to overexpress the gene for the conserved aerobic sn-glycerol-3-phosphate dehydrogenase GlpD. The GlpD overexpression strain showed increased tolerance to ampicillin and ofloxacin, while a strain with glpD deleted had a decreased level of persisters in the stationary state. This suggests that GlpD is a component of the MDT mechanism. Further genetic studies of mutants affected in pathways involved in sn-glycerol-3-phosphate metabolism have led to the identification of two additional multidrug tolerance loci, glpABC, the anaerobic sn-glycerol-3-phosphate dehydrogenase, and plsB, an sn-glycerol-3-phosphate acyltransferase.


* Corresponding author. Mailing address: Northeastern University, Department of Biology, 405 Mugar Hall, 360 Huntington Ave., Boston, MA 02115. Phone: (617) 373-8238. Fax: (617) 373-3724. E-mail: klewis{at}neu.edu.

{dagger} Present address: Schepens Eye Research Institute, 20 Staniford St., Boston, MA 02115.


Journal of Bacteriology, July 2006, p. 5136-5144, Vol. 188, No. 14
0021-9193/06/$08.00+0     doi:10.1128/JB.00369-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Harrison, J. J., Wade, W. D., Akierman, S., Vacchi-Suzzi, C., Stremick, C. A., Turner, R. J., Ceri, H. (2009). The Chromosomal Toxin Gene yafQ Is a Determinant of Multidrug Tolerance for Escherichia coli Growing in a Biofilm. Antimicrob. Agents Chemother. 53: 2253-2258 [Abstract] [Full Text]  
  • Hansen, S., Lewis, K., Vulic, M. (2008). Role of Global Regulators and Nucleotide Metabolism in Antibiotic Tolerance in Escherichia coli. Antimicrob. Agents Chemother. 52: 2718-2726 [Abstract] [Full Text]  
  • Anderson, G. G., Moreau-Marquis, S., Stanton, B. A., O'Toole, G. A. (2008). In Vitro Analysis of Tobramycin-Treated Pseudomonas aeruginosa Biofilms on Cystic Fibrosis-Derived Airway Epithelial Cells. Infect. Immun. 76: 1423-1433 [Abstract] [Full Text]  
  • Palmer, R. J. Jr., Stoodley, P. (2007). Biofilms 2007: Broadened Horizons and New Emphases. J. Bacteriol. 189: 7948-7960 [Full Text]  
  • Klapper, I., Gilbert, P., Ayati, B. P., Dockery, J., Stewart, P. S. (2007). Senescence can explain microbial persistence. Microbiology 153: 3623-3630 [Abstract] [Full Text]  
  • Correia, F. F., D'Onofrio, A., Rejtar, T., Li, L., Karger, B. L., Makarova, K., Koonin, E. V., Lewis, K. (2006). Kinase Activity of Overexpressed HipA Is Required for Growth Arrest and Multidrug Tolerance in Escherichia coli. J. Bacteriol. 188: 8360-8367 [Abstract] [Full Text]