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 Helling, R. B.
Right arrow Articles by Miller, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Helling, R. B.
Right arrow Articles by Miller, C.

 Previous Article  |  Next Article 

Journal of Bacteriology, July 2002, p. 3699-3703, Vol. 184, No. 13
0021-9193/02/$04.00+0     DOI: 10.1128/JB.184.13.3699-3703.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Toxic Waste Disposal in Escherichia coli

Robert B. Helling,* Brian K. Janes, Heather Kimball, Timothy Tran, Michael Bundesmann, Pietra Check, Darcy Phelan, and Charles Miller

Department of Biology, University of Michigan, Ann Arbor, Michigan 48109-1048

Received 22 November 2000/ Accepted 2 April 2002

About 10% of the nalidixic acid-resistant (Nalr) mutants in a transposition-induced library exhibited a growth factor requirement as the result of cysH, icdA, metE, or purB mutation. Resistance in all of these mutants required a functional AcrAB-TolC efflux pump, but the EmrAB-TolC pump played no obvious role. Transcription of acrAB was increased in each type of Nalr mutant. In the icdA and purB mutants, each of the known signaling pathways appeared to be used in activating the AcrAB-TolC pump. The metabolites that accumulate upstream of the blocks caused by the mutations are hypothesized to increase the levels of the AcrAB-TolC pump, thereby removing nalidixic acid from the organism.


* Corresponding author. Mailing address: Department of Biology, University of Michigan, Natural Science Building, 830 N. University, Ann Arbor, MI 48109-1048. Phone: (734) 764-1455. Fax: (734) 647-0884. E-mail: helling{at}umich.edu.


Journal of Bacteriology, July 2002, p. 3699-3703, Vol. 184, No. 13
0021-9193/02/$04.00+0     DOI: 10.1128/JB.184.13.3699-3703.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Rosner, J. L., Martin, R. G. (2009). An Excretory Function for the Escherichia coli Outer Membrane Pore TolC: Upregulation of marA and soxS Transcription and Rob Activity Due to Metabolites Accumulated in tolC Mutants. J. Bacteriol. 191: 5283-5292 [Abstract] [Full Text]  
  • Poole, K. (2005). Efflux-mediated antimicrobial resistance. J Antimicrob Chemother 56: 20-51 [Abstract] [Full Text]  
  • Lomovskaya, O., Totrov, M. (2005). Vacuuming the Periplasm. J. Bacteriol. 187: 1879-1883 [Full Text]  
  • Lin, J., Akiba, M., Sahin, O., Zhang, Q. (2005). CmeR Functions as a Transcriptional Repressor for the Multidrug Efflux Pump CmeABC in Campylobacter jejuni. Antimicrob. Agents Chemother. 49: 1067-1075 [Abstract] [Full Text]  
  • Sobel, M. L., Neshat, S., Poole, K. (2005). Mutations in PA2491 (mexS) Promote MexT-Dependent mexEF-oprN Expression and Multidrug Resistance in a Clinical Strain of Pseudomonas aeruginosa. J. Bacteriol. 187: 1246-1253 [Abstract] [Full Text]  
  • Van Dyk, T. K., Templeton, L. J., Cantera, K. A., Sharpe, P. L., Sariaslani, F. S. (2004). Characterization of the Escherichia coli AaeAB Efflux Pump: a Metabolic Relief Valve?. J. Bacteriol. 186: 7196-7204 [Abstract] [Full Text]