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

青枯雷尔氏菌在寄主植物中增殖机制的研究-青枯雷尔氏菌与寄主植物相互作用的综合分析-

基本信息

批准号：
16380037
负责人：
HIKICHI Yasufumi
金额：
$ 10.18万
依托单位：
Kochi University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2004
资助国家：
日本
起止时间：
2004 至 2005
项目状态：
已结题

项目摘要

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.

青枯病是世界范围内最具破坏性的植物病害之一。R.青枯菌首先侵入根的细胞间隙。在细胞间隙增殖后，细菌侵入木质部导管并产生胞外多糖（EPS），导致受感染植物枯萎。R.青枯菌具有过敏反应和致病性（hrp）基因，编码III型分泌系统（TTSS）。致病性的R.青枯菌需要细菌在细胞间隙增殖，这取决于宿主植物和III型效应子之间的相互作用。hrpB不仅调节hrp的表达，而且还调节编码外蛋白的基因的表达，例如通过II型分泌系统（TWSS）分泌的聚半乳糖醛酸酶PehC。TWSS的破坏影响TTSS的功能，提示TTSS和TWSS在功能上存在相互作用。当细菌细胞密度超过2 × 10^7 cfu/ml时，通过群体感应激活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，红曲霉的致病性较弱。青枯菌通过细菌在细胞间隙中的增殖，通过致病因子之间的相互调节来进行全局调节。