Studies on mechanism of Ralstoniia solanacearum proliferation in host plants - Comprehensive analysis of interaction between R.solanacearum and host plants -

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Bacterial wilt caused by Ralstonia solanacearum is one of the most devastating plant diseases worldwide. R. solanacearum first invades intercellular spaces of roots. After multiplication in intercellular spaces, the bacteria invade xylem vessels and produce exopolysaccharide (EPS), leading to wilt of the infected plants. R. solanacearum possesses hypersensitive response and pathogenicity (hrp) genes, which encodes the type III secretion system (TTSS). Pathogenicity of R. solanacearum required multiplication of the bacteria in intercellular spaces, which was dependent on interactions between host plants and type III effectors. HrpB regulated expression of not only hrp but also genes encoding exoprotein such as polygalacuturonase PehC secreted through type II secretion system (TWSS). Disruption of TWSS influenced function of TTSS, suggesting interaction between TTSS and TWSS on their functions. PhcA activated by a quorum-sensing in response to bacterial cell density at more than 2 × 10^7 cfu/ml induced expression of xpsR, leading to biosynthesis of EPS. Moreover, active PhcA also suppressed expression of prhIR, resulting in suppression of hrp expression. These results suggest that pathogenicity of R. solanacearum is globally regulated by mutual regulation among pathogenicity factors through multiplication of the bacteria in intercellular spaces.