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Journal of Bacteriology, December 2008, p. 8163-8170, Vol. 190, No. 24
0021-9193/08/$08.00+0     doi:10.1128/JB.01181-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Loss of a Biofilm-Inhibiting Glycosyl Hydrolase during the Emergence of Yersinia pestis{triangledown}

David L. Erickson,1* Clayton O. Jarrett,1 Julie A. Callison,1 Elizabeth R. Fischer,2 and B. Joseph Hinnebusch1

Laboratory of Zoonotic Pathogens,1 RTS Microscopy Unit, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 903 S. 4th St., Hamilton, Montana 598402

Received 20 August 2008/ Accepted 3 October 2008

Yersinia pestis, the bacterial agent of plague, forms a biofilm in the foregut of its flea vector to produce a transmissible infection. The closely related Yersinia pseudotuberculosis, from which Y. pestis recently evolved, can colonize the flea midgut but does not form a biofilm in the foregut. Y. pestis biofilm in the flea and in vitro is dependent on an extracellular matrix synthesized by products of the hms genes; identical genes are present in Y. pseudotuberculosis. The Yersinia Hms proteins contain functional domains present in Escherichia coli and Staphylococcus proteins known to synthesize a poly-β-1,6-N-acetyl-D-glucosamine biofilm matrix. In this study, we show that the extracellular matrices (ECM) of Y. pestis and staphylococcal biofilms are antigenically related, indicating a similar biochemical structure. We also characterized a glycosyl hydrolase (NghA) of Y. pseudotuberculosis that cleaved β-linked N-acetylglucosamine residues and reduced biofilm formation by staphylococci and Y. pestis in vitro. The Y. pestis nghA ortholog is a pseudogene, and overexpression of functional nghA reduced ECM surface accumulation and inhibited the ability of Y. pestis to produce biofilm in the flea foregut. Mutational loss of this glycosidase activity in Y. pestis may have contributed to the recent evolution of flea-borne transmission.

* Corresponding author. Present address: Department of Microbiology and Molecular Biology, Brigham Young University, Provo, UT 84663. Phone: (801) 422-1981. Fax: (801) 422-0519. E-mail: xenopsylla{at}gmail.com

{triangledown} Published ahead of print on 17 October 2008.

Journal of Bacteriology, December 2008, p. 8163-8170, Vol. 190, No. 24
0021-9193/08/$08.00+0     doi:10.1128/JB.01181-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Zhou, D., Yang, R. (2009). Molecular Darwinian Evolution of Virulence in Yersinia pestis. Infect. Immun. 77: 2242-2250 [Full Text]  


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