Only 25 genes were aberrant in at least one strain, among which 9 usual suspects from the CPS locus, but also four hemagglutinins. Figure 3 Virulence associated genes in the conserved core selleck compound genome of P. gingivalis. A. 153 potential virulence

genes from the genome annotation of W83 combined with the conserved core genome of P. gingivalis [29]. B 39 genes known to be up-regulated during infection combined with the conserved core genome of P. gingivalis [46, 47]. The number in the overlapping part of the circles is the number of potential virulence associated genes that was found in the conserved core genome of P. gingivalis. Another virulence gene set was also tested for presence in the conserved core gene set of P. gingivalis. The set was composed of genes shown to be PLX3397 chemical structure up-regulated in infection experiments [46, 47]. Genes up-regulated in an in vitro human epithelial cell infection experiment were combined with a gene set in vivo up-regulated on protein level in a mouse subcutanuous chamber experiment to

make a set of 39 virulence genes. The former experiment was chosen as an early response gene set, whereas the latter includes genes involved in sustaining an infection Selleck CFTRinh-172 in vivo. 37 of the 39 virulence genes were present among the core gene set (Figure 3B). The two genes that were not in the core gene set were a thiol protease (PG1055) [48] and tetR a transcription regulator (PG1240). The thiol protease is aberrant in each strain except for strain ATCC49417, from the 16S-23S ISR heteroduplex type that together with the type of strain W83 has the highest association with disease [49]. This is another indication that this thiol protease may be an important determinant Isotretinoin in virulence of P. gingivalis. Transcription regulator tetR was only found

to be aberrant in strain FDC381, which is the least virulent and the only non-encapsulated strain [18, 32]. The analysis of the core gene set shows the presence of almost all virulence related genes. The genes that are not present in the core genome may be determinants of the differences in virulence found between the strains. Strain divergence The divergences of the test strains were determined by the percentage of aberrant CDSs from the total number of 1874 CDSs included in this study. We found 8.2% to 13.7% of aberrant genes per strain, with ATCC49417 having the lowest and FDC381 having the highest percentage of aberrant genes (Table 4). These percentages of aberrant genes are higher than the 7% of aberrant genes from a previous genomic hybridization study on strain ATCC33277, a close relative of strain FDC381 [25]. From the 64 highly aberrant genes in ATCC33277 41 genes were included in our study from which 33 were in the aberrant gene list of strain FDC381.