Novel DNA binding protein of Treponema denticola regulates the response against oxygen stress and be associated with expression of virulence factors
Oxygen is a fatal stress for periodontal pathogenic bacteria composed of obligate anaerobes. Although Treponema denticola is a major pathogen of periodontitis, it remains unclear the mechanism of oxygen stress responses. T. denticola gene, TDE_0127, was reported to be upregulated by oxygen exposure. However, its exact function has not yet been clarified. The purpose of this study was to investigate the potential involvement of TDE_0127 in oxygen stress response and the virulence of T. denticola. To investigate its function, we constructed, for the first time, a mutant strain deficient in TDE_0127 by homologous recombination. Viable cell proportion under aerobic condition was evaluated by ATP-based assay. Gene expression profile of the mutant strain was evaluated by RNA-seq. Dentilisin activity was evaluated using a synthetic substrate. Under aerobic conditions, the proportion of viable cells in the mutant strain was reduced by approximately 40% as compared to wild type strain (p<0.05), indicating that inactivation of TDE_0127 attenuates resistance to oxygen exposure. The results of RNA-seq showed that 153 genes including peroxiredoxin (TDE_0011) significantly reduced in the mutant (p<0.01) and 38 genes including internalin-related protein (TDE_2231) was increased (p<0.01). In addition, dentilisin activity in the mutant strain decreased approximately 30% compared to the wild-type strain (p<0.05). These results suggest that T. denticola TDE_0127 is involved in the resistance to oxygen stress, activation of dentilisin and regulation of the expression of a Lrr protein.