| Ralstonia solanacearum, the causative agent of bacterial wilt disease, is arguably one of the most destructive bacterial plant pathogens due to its large host range, wide geographical distribution, and lack of effective control methods. Many virulence factors have been identified, providing useful insight into this pathogen and disease development. However, little is known about how R. solanacearum adapts to effectively colonize and cause disease in its hosts. A recent in vivo expression technology (IVET) study suggested that R. solanacearum encounters oxidative stress during mid-phase tomato pathogenicity. I hypothesized that R. solanacearum expresses oxidative stress response genes during pathogenesis and that these genes are necessary for growth, survival, adaptation, and disease development in host plants.;In this thesis I describe my findings on the R. solanacearum oxidative stress response and its role in virulence. R. solanacearum is exposed to reactive oxygen species during host infection and possesses multiple and redundant predicted reactive oxygen species-scavenging enzymes. Mutagenesis of the plant induced gene bcp demonstrated that it encodes a peroxidase that plays a small role in bacterial wilt disease. However, mutagenesis of the only apparent regulator of the oxidative stress response, OxyR, resulted in a strain that was severely affected in virulence, suggesting that R. solanacearum encounters potentially inhibitory levels of oxidative stress during normal disease progress. Expression studies revealed that OxyR-regulated genes in R. solanacearum are similar to those in other bacteria including katE, katG, ahpC1, grxC and itself. In addition, some of my results point to the presence of a second regulator of the oxidative stress response; this regulator is yet to be identified. The work presented in this thesis demonstrates that R. solanacearum is exposed to reactive oxygen species during pathogenesis and that an effective oxidative stress response is necessary for bacterial wilt disease. |
