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Name Bench ID Date MICR3004


Higher order taxa

Bacteria – Bacteroidetes – Bacteroidia – Bacteroidales – Porphyromonadaceae - Porphyromonas - P. gingivalis


Species: Porphyromonas gingivalis Strain: W88

Description and significance

Puzzle globe
Gram negative cell wall structure

Genome structure

The genome of strain W88 is comprised of a circular chromosome made up of 2 343 479 bp’s. On average the guanine and cytosine content make up approximately 48.3 % of the genome. The circular chromosome encodes 1909 protein genes 65 RNA genes. 4 ribosomal operons (rrn, 5S rRNA-23S rRNA-tRNAAla-tRNAIle-16S rRNA) including 53 tRNA genes showing specificity for all 20 amino acids have been documented. Interestingly the number of rrn operons and tRNA genes in strain W83 were identical to those of an avirulent strain counterpart ATCC 33277. Nonetheless the extensive rearrangement between the two strains through the introduction of mobile elements inevitably altered the virulence of the bacterium.

The genome of W83 is composed predominately (85%) of ORF. Encoding a total of 1,990 ORF, 1075 presented detectable biological roles. Of the remaining ORF, 184 were categorised as a conserved hypothetical protein or conserved domain protein, 208 had to known function, and 523 encoded hypothetical proteins.

Cell structure and metabolism

Cell Wall: P. gingivalis is an obligately aerobic, non-motile gram-negative bacterium (2). Its cell wall is characterised by three distinct layers, including two membranous structures known as the inner membrane (IM) and the outer membrane (OM) (11). Connecting the two layers is a gel like structure known as the periplasm and a thin layer of peptidoglycan (11). The IM and OM possess a trilamellar structure composed of phospholipids (11). Distributed along the outer membrane are lipoproteins and lipopolysaccharides (LPS), which serve as an anchor for lipids (11). Chemically LPS is composed of three subunits, the O specific polysaccharide chain, the core and lipid A (11).

Puzzle globe
Gram negative cell wall structure

Fimbriae: Protruding the outer membrane of the cell wall, thin proteinaceous surface appendages aid and mediate bacterial attachment to the host (12). Approximately 25 μm long (12) these structures have a robust ability to interact with salivary proteins, epithelial cells, extracellular matrix proteins and the fibroblasts of the host. Two distinct fimbriae types are displayed on the cell surfaces of the bacteria, known as FimA and Mfa protein (12). These surface structures are proposed to have a role in the progression of periodontal inflammatory reactions. Six genotypes of FimA structures exist (type I-V and Ib), ranging from 40.5 to 49kDa in size (12). Strain W83 is classed under type IV and are poorly fimbriated whereas strain ATCC 33277 are an abundantly fimbriated type I strain (12). The progression of chronic periodontitis is most closely associated with type II strains followed by type IV (12).

Biofilm formation: The bacterium colonises the oral cavity by forming a complex biofilm known as plaque (5). They are recognised as secondary or late colonisers and require antecedent organisms to form the necessary environmental conditions for growth (12). Upon contact the bacterium must resist the plethora of host responses working against bacterial colonisation (5). Host factors are known to include mechanical shearing produced from the force of the tongue, saliva and gingival crevicular fluid flow (5). Successful colonisers must therefore possess a diverse repertoire of virulence factors to overcome host defences (5).

Motility: Non-motile

Metabolic Functions: P. gingivalis is dependent on nitrogenous substrates for energy production (5). Despite the nitrogenous compounds present in the oral cavity, the bacterium has a limited ability to ferment free amino acids. Aspartic acid and Asparagine are among the few, which can be metabolised to yield succinate.



Application to biotechnology

Bioengineering, biotechnologically relevant enzyme/compound production, drug targets,…

Current research

Summarise some of the most recent discoveries regarding this species.



1. Boone D, R and Castenholtz R, W. Bergey's Manual of Systematic Bacteriology. 2nd Ed. Vol. 1. Springer-Verlag: New York; 2002.

2. Shah N, H., Collins D, M. (1988) Proposal for Reclassification of Bacteroides asaccharolyticus, Bacteroides gingivalis, and Bacteroides endodontalis in a New Genus, Porphyromonas. Int J Syst Evol Microbiol 38 :128-131.

3. Naito, M., Hirakawa, H., Yamashita, A., Ohara, N., Shoji, M., Yukitake, H., Nakayama, K., Toh, H., Yoshimura, F., Kuhara, S., Hattori, M., Hayashi, T., Nakayama, K. (2008) Determination of the genome sequence of Porphyromonas gingivalis strain ATCC 33277 and genomic comparison with strain W83 revealed extensive genome rearrangements in P. gingivalis. DNA Res 15 :215-225.

4. Ohara-Nemoto, Y., Rouf, S. M., Naito, M., Yanase, A., Tetsuo, F., Ono, T., Kobayakawa, T., Shimoyama, Y., Kimura, S., Nakayama, K., Saiki, K., Konishi, K. & Nemoto, T. K. (2014) Identification and characterization of prokaryotic dipeptidyl-peptidase 5 from Porphyromonas gingivalis. J Biol Chem, 289: 5436-48.

5. Lamont, R. J. & Jenkinson, H. F. (1998) Life below the gum line: pathogenic mechanisms of Porphyromonas gingivalis. Microbiol Mol Biol Rev, 62: 1244-63.

6. Igboin, C. O., Griffen, A. L. and Leys, E. J. (2009) Porphyromonas gingivalis strain diversity. J Clin Microbiol, 47,: 3073-81.

7. Grenier, D. and Mayrand, D. 1987. Selected characteristics of pathogenic and nonpathogenic strains of Bacteroides gingivalis. J Clin Microbiol, 25: 738-40.

8. [1]

9. [2]

11. Chatterjee. S and Chaudhuri K. (2012) Outer membrane vesicles of bacteria. SpringerBriefs in Microbiology

  • Chapter Book

12. How, K. Y., Song, K. P. and Chan, K. G. (2016) Porphyromonas gingivalis: An Overview of Periodontopathic Pathogen below the Gum Line. Front Microbiol, 7: 53.

13. Bao, K., Belibasakis, G. N., Thurnheer, T., Aduse-Opoku, J., Curtis, M. A. and Bostanci, N. (2014) Role of Porphyromonas gingivalis gingipains in multi-species biofilm formation. BMC Microbiol, 14: 258.

14. Cugini, C., Klepac-Ceraj, V., Rackaityte, E., Riggs, J. E. and Davey, M. E. (2013. Porphyromonas Gingivalis: Keeping The Pathos Out Of The Biont. J Oral Microbiol, 5.

15. Goulbourne, P. A. and Ellen, R. P. (1991) Evidence that Porphyromonas (Bacteroides) gingivalis fimbriae function in adhesion to Actinomyces viscosus. J Bacteriol, 173: 5266-74.

16. Jenkinson, H. F. and Demuth, D. R. (1997) Structure, function and immunogenicity of streptococcal antigen I/II polypeptides. Mol Microbiol, 23: 183-90.

17. Lamont, R. J., Gil, S., Demuth, D. R., Malamud, D. and Rosan, B. (1994) Molecules of Streptococcus gordonii that bind to Porphyromonas gingivalis. Microbiology, 140: 867-72.

18. Nagata, H., Murakami, Y., Inoshita, E., Shizukuishi, S. and Tsunemitsu, A. (1990) Inhibitory effect of human plasma and saliva on co-aggregation between Bacteroides gingivalis and Streptococcus mitis. J Dent Res, 69: 1476-9.

19. Lewis, J. P., Iyer, D. and Anaya-Bergman, C. (2009) Adaptation of Porphyromonas gingivalis to microaerophilic conditions involves increased consumption of formate and reduced utilization of lactate. Microbiology, 155: 3758-74.

20. K. E., Fleischmann, R. D., Deboy, R. T., Paulsen, I. T., Fouts, D. E., Eisen, J. A., Daugherty, S. C., Dodson, R. J., Durkin, A. S., Gwinn, M., Haft, D. H., Kolonay, J. F., Nelson, W. C., Mason, T., Tallon, L., Gray, J., Granger, D., Tettelin, H., Dong, H., Galvin, J. L., Duncan, M. J., Dewhirst, F. E. and Fraser, C. M. (2003) Complete genome sequence of the oral pathogenic Bacterium porphyromonas gingivalis strain W83. J Bacteriol, 185: 5591-601.

21. Mysak, J., Podzimek, S., Sommerova, P., Lyuya-Mi, Y., Bartova, J., Janatova, T., Prochazkova, J. and Duskova, J. (2014) Porphyromonas gingivalis: major periodontopathic pathogen overview. J Immunol Res, 2014: 476068.

This page is written by Amy Pham for the MICR3004 course, Semester 2, 2016