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Infection and Immunity, November 2006, p. 6145-6153, Vol. 74, No. 11
0019-9567/06/$08.00+0     doi:10.1128/IAI.00261-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Porphyromonas gingivalis galE Is Involved in Lipopolysaccharide O-Antigen Synthesis and Biofilm Formation{triangledown}

Ryoma Nakao,* Hidenobu Senpuku, and Haruo Watanabe

Department of Bacteriology, National Institute of Infectious Diseases, Tokyo, Japan 162-8640

Received 17 February 2006/ Returned for modification 22 May 2006/ Accepted 25 August 2006

Porphyromonas gingivalis is a crucial component of complex plaque biofilms that form in the oral cavity, resulting in the progression of periodontal disease. To elucidate the mechanism of periodontal biofilm formation, we analyzed the involvement of several genes related to the synthesis of polysaccharides in P. gingivalis. Gene knockout P. gingivalis mutants were constructed by insertion of an ermF-ermAM cassette; among these mutants, the galE mutant showed some characteristic phenotypes involved in the loss of GalE activity. As expected, the galE mutant accumulated intracellular carbohydrates in the presence of 0.1% galactose and did not grow in the presence of galactose at a concentration greater than 1%, in contrast to the parental strain. Lipopolysaccharide (LPS) analysis indicated that the length of the O-antigen chain of the galE mutant was shorter than that of the wild type. It was also demonstrated that biofilms generated by the galE mutant had an intensity 4.5-fold greater than those of the wild type. Further, the galE mutant was found to be significantly susceptible to some antibiotics in comparison with the wild type. In addition, complementation of the galE mutation led to a partial recovery of the parental phenotypes. We concluded that the galE gene plays a pivotal role in the modification of LPS O antigen and biofilm formation in P. gingivalis and considered that our findings of a relationship between the function of the P. gingivalis galE gene and virulence phenotypes such as biofilm formation may provide clues for understanding the mechanism of pathogenicity in periodontal disease.

* Corresponding author. Mailing address: Department of Bacteriology, National Institute of Infectious Diseases, 1-23-1, Toyama, Shinjuku-ku, Tokyo, Japan 162-8640. Phone: 81-3-5285-1111. Fax: 81-3-5285-1163. E-mail: ryoma73{at}nih.go.jp.

{triangledown} Published ahead of print on 5 September 2006.

Editor: V. J. DiRita

Infection and Immunity, November 2006, p. 6145-6153, Vol. 74, No. 11
0019-9567/06/$08.00+0     doi:10.1128/IAI.00261-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Mazumdar, V., Snitkin, E. S., Amar, S., Segre, D. (2009). Metabolic Network Model of a Human Oral Pathogen. J. Bacteriol. 191: 74-90 [Abstract] [Full Text]  


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