抄録
Ralstonia 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. R. solanacearum strain OE1-1 (OE1-1), which is pathogenic to tobacco, possessed hrp encoding the type III secretion system (T3SS), and its pathogenicity depended on interactions between the host plants and type III effectors. HrpB positively regulated expression of not only hrpbut also genes encoding exoproteins secreted through the type II secretion system (T2SS), such as an exo-polygalacturonase, PehC. A consortium of T2SS-secreted plant cell wall-degrading enzymes contributed to not only invasion of xylem vessels, leading to systemic infection, but also quantitative control of virulence. PhcA activated by quorum sensing in response to the bacterial cell density induces biosynthesis of EPS. Moreover, active PhcA also suppressed expression of the prhR/prhI operon, resulting in suppression of hrp expression. Therefore, R. solanacearum pathogenicity is globally regulated by mutual regulation by pathogenicity factors through multiplication of the bacteria.
