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Antimicrobial Agents and Chemotherapy, June 2009, p. 2253-2258, Vol. 53, No. 6
0066-4804/09/$08.00+0     doi:10.1128/AAC.00043-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

The Chromosomal Toxin Gene yafQ Is a Determinant of Multidrug Tolerance for Escherichia coli Growing in a Biofilm{triangledown}

Joe J. Harrison,1,2,{dagger} William D. Wade,1,2 Sarah Akierman,1 Caterina Vacchi-Suzzi,1,2 Carol A. Stremick,1,2 Raymond J. Turner,1* and Howard Ceri1,2*

Department of Biological Sciences, University of Calgary, 2500 University Drive N.W., Calgary, AB, Canada T2N 1N4,1 Biofilm Research Group, University of Calgary, 2500 University Drive N.W., Calgary, AB, Canada T2N 1N42

Received 12 January 2009/ Returned for modification 28 February 2009/ Accepted 14 March 2009

Escherichia coli is refractory to elevated doses of antibiotics when it is growing in a biofilm, and this is potentially due to high numbers of multidrug-tolerant persister cells in the surface-adherent population. Previously, the chromosomal toxin-antitoxin loci hipBA and relBE have been linked to the frequency at which persister cells occur in E. coli populations. In the present study, we focused on the dinJ-yafQ-encoded toxin-antitoxin system and hypothesized that deletion of the toxin gene yafQ might influence cell survival in antibiotic-exposed biofilms. By using confocal laser scanning microscopy and viable cell counting, it was determined that a {Delta}yafQ mutant produced biofilms with a structure and a cell density equivalent to those of the parental strain. In-depth susceptibility testing identified that relative to wild-type E. coli, the {Delta}yafQ strain had up to a ~2,400-fold decrease in cell survival after the biofilms were exposed to bactericidal concentrations of cefazolin or tobramycin. Corresponding to these data, controlled overexpression of yafQ from a high-copy-number plasmid resulted in up to a ~10,000-fold increase in the number of biofilm cells surviving exposure to these bactericidal drugs. In contrast, neither the inactivation nor the overexpression of yafQ affected the tolerance of biofilms to doxycycline or rifampin (rifampicin). Furthermore, deletion of yafQ did not affect the tolerance of stationary-phase planktonic cells to any of the antibacterials tested. These results suggest that yafQ mediates the tolerance of E. coli biofilms to multiple but specific antibiotics; moreover, our data imply that this cellular pathway for persistence is likely different from that of multidrug-tolerant cells in stationary-phase planktonic cell cultures.

* Corresponding author. Mailing address: Department of Biological Sciences, University of Calgary, 2500 University Drive N.W., Calgary, AB, Canada T2N 1N4. Phone for Raymond J. Turner: (403) 220-4308. Fax: (403) 289-9311. E-mail: turnerr{at}ucalgary.ca. Phone for Howard Ceri: (403) 220-6960. Fax: (403) 289-9311. E-mail: ceri{at}ucalgary.ca

{triangledown} Published ahead of print on 23 March 2009.

{dagger} Present address: Department of Microbiology, University of Washington, Box 357242, 1959 NE Pacific Street, Seattle, WA 98195-7242.

Antimicrobial Agents and Chemotherapy, June 2009, p. 2253-2258, Vol. 53, No. 6
0066-4804/09/$08.00+0     doi:10.1128/AAC.00043-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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