Abstract
Bacterial wilt caused by Ralstonia solanacearum is one of the most devastating plant diseases worldwide. R. solanacearum first invades intercellular spaces of roots where it multiplies before invading xylem vessels and producing exopolysaccharide (EPS), leading to wilt of the infected plant. In this review, we focus on regulation of R. solanacearum pathogenicity, which requires proliferation in intercellular spaces. R. solanacearum possesses hrp encoding the type III secretion system (T3SS), and its pathogenicity depends on interactions between the host plant and type III effectors. HrpB positively regulates expression of not only hrp but also genes encoding exoproteins secreted through the type II secretion system (T2SS). A consortium of T2SS-secreted exocellular proteins containing plant cell wall-degrading enzymes contributes to not only invasion of xylem vessels, leading to systemic infection, but also quantitative control of virulence. Moreover, T2SS functionally interacts with T3SS. PhcA activated by quorum sensing in response to the bacterial cell density induces expression of xpsR, leading to biosynthesis of EPS. Moreover, active PhcA also suppresses expression of prhIR, resulting in suppression of hrp expression. These results suggest that R. solanacearum pathogenicity is globally regulated by mutual regulation by pathogenicity factors through multiplication of the bacteria in intercellular spaces.
