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Infection and Immunity, September 2009, p. 3522-3532, Vol. 77, No. 9
0019-9567/09/$08.00+0     doi:10.1128/IAI.00036-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Transcriptional Profiling Identifies the Metabolic Phenotype of Gonococcal Biofilms{triangledown} ,{dagger}

Megan L. Falsetta,1 Thomas B. Bair,1 Shan Chi Ku,2 Rachel N. vanden Hoven,2 Christopher T. Steichen,1 Alastair G. McEwan,2 Michael P. Jennings,2 and Michael A. Apicella1*

Department of Microbiology, The University of Iowa, Iowa City, Iowa 52242,1 School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane QLD 4072, Australia2

Received 9 January 2009/ Returned for modification 16 March 2009/ Accepted 5 June 2009

Neisseria gonorrhoeae, the etiologic agent of gonorrhea, is frequently asymptomatic in women, often leading to chronic infections. One factor contributing to this may be biofilm formation. N. gonorrhoeae can form biofilms on glass and plastic surfaces. There is also evidence that biofilm formation may occur during natural cervical infection. To further study the mechanism of gonococcal biofilm formation, we compared transcriptional profiles of N. gonorrhoeae biofilms to planktonic profiles. Biofilm RNA was extracted from N. gonorrhoeae 1291 grown for 48 h in continuous-flow chambers over glass. Planktonic RNA was extracted from the biofilm runoff. In comparing biofilm with planktonic growth, 3.8% of the genome was differentially regulated. Genes that were highly upregulated in biofilms included aniA, norB, and ccp. These genes encode enzymes that are central to anaerobic respiratory metabolism and stress tolerance. Downregulated genes included members of the nuo gene cluster, which encodes the proton-translocating NADH dehydrogenase. Furthermore, it was observed that aniA, ccp, and norB insertional mutants were attenuated for biofilm formation on glass and transformed human cervical epithelial cells. These data suggest that biofilm formation by the gonococcus may represent a response that is linked to the control of nitric oxide steady-state levels during infection of cervical epithelial cells.

* Corresponding author. Mailing address: Department of Microbiology, The University of Iowa, 51 Newton Rd., BSB 3-403, Iowa City, IA 52242. Phone: (319) 335-7807. Fax: (319) 335-9006. E-mail: michael-apicella{at}uiowa.edu

{triangledown} Published ahead of print on 15 June 2009.

{dagger} Supplemental material for this article may be found at http://iai.asm.org/.

Editor: J. N. Weiser

Infection and Immunity, September 2009, p. 3522-3532, Vol. 77, No. 9
0019-9567/09/$08.00+0     doi:10.1128/IAI.00036-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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