These 22 probes are called dead probes as they do not give any significant hybridization signal. Table 3 Dead probes excluded from the results due to low hybridization signals GeneID Annotated function PG0222 DNA-binding protein, histone-like family PG0375 ribosomal protein L13 PG0498 autoinducer-2 production protein LuxS PG0786 hypothetical protein PG0809 hypothetical protein PG0855 hypothetical protein PG0880 bacterioferritin comigratory protein PG0979 hypothetical protein PG0994 hypothetical protein PG1234 hypothetical protein PG1257 hypothetical click here protein PG1335 membrane protein, putative PG1357 hypothetical protein
PG1412 ISPg2, transposase, truncation PG1617 hypothetical protein PG1660 RNA polymerase sigma-70 factor, ECF subfamily PG1742 hypothetical protein PG1866 hypothetical protein PG1869 hypothetical protein PG1987 CRISPR-associated protein, TM1794 family PG2019 hypothetical protein PG2087 conserved hypothetical protein In order to maximize the mining of the genomic information, we subjected the check details data to three complementary analyses: 1) analysis for aberrations as detected by individual probes, 2) analysis for breakpoints, and 3) analysis for genomic loss. The rationale behind the three Selleck AZD2281 analyses is as follows. The probed genomic sites are on average 1250 bp apart from
each other (median was 1018), which was not considered to be a high interrogation density. We therefore decided to analyze each probe individually for indication that the genomic site interrogated is aberrant from W83. Deviations from W83 that were detected with a
false discovery rate corrected p-value (FDR) < 0.05 were considered significant. This aberrance could have occurred due to mutations or loss (or due to W83 gain), and this was regarded as point-variability between the strains. Nevertheless, if several neighboring probes indicate aberrations, then this may indicate highly variable regions due to mutations or loss. Hence, a breakpoint analysis Rucaparib in vivo was executed to quantitatively specify such regions. Finally, we used the negative controls to define absent calls with the aim to distinguish whether an aberration was found more likely due to mutation or loss. If the probes that indicated aberrations in the first analysis also showed the same intensities as the negative controls with FDR corrected p-value < 0.01 (see M&M), the genomic site was considered as mutated, and otherwise it was considered as lost. This last analysis enhanced our interpretation of the data and the definition of the core genome. P. gingivalis core genome Research on microbial pathogens is mostly performed to unravel mechanisms of virulence in order to design effective treatments. Virulence mechanisms present in all strains of a species are especially attractive. The description of a core set of genes present in a species is thus a key step for better understanding. From an analysis of eight P.