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

青枯病是世界范围内危害最严重的植物病害之一。青枯病菌首先侵入根部的细胞间隙。细菌在细胞间隙中繁殖后，侵入木质部导管并产生胞外多糖(EPS)，导致受感染植物的枯萎。青枯菌具有超敏反应和致病性(Hrp)基因，编码III型分泌系统(TTSS)。青枯病菌的致病需要细菌在细胞间隙内繁殖，这依赖于寄主植物和III型效应器之间的相互作用。HrpB不仅调节HRP的表达，而且还调节编码外源蛋白的基因的表达，如通过II型分泌系统(TWSS)分泌的多聚半乳尿苷酸酶PehC。TWSS的破坏影响了TTSS的功能，提示TTSS和TWSS之间存在相互作用。当菌体密度大于2×10~(-7)cfu/ml时，群体感应激活的PhcA诱导xpsR的表达，导致EPS的生物合成。此外，活性PhcA还抑制了prhIR的表达，从而抑制了HRP的表达。这些结果表明，青枯菌的致病力是由致病因子之间通过细菌在细胞间隙中的繁殖而相互调节的。

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.