| Project/Area Number |
16380037
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Plant pathology
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| Research Institution | Kochi University |
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Principal Investigator |
HIKICHI Yasufumi Kochi University, Faculty of Agriculture, Professor, 農学部, 教授 (70291507)
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| Co-Investigator(Kenkyū-buntansha) |
KIBA Akinori Kochi University, Faculty of Agriculture, Associate Professor, 農学部, 助教授 (50343314)
OHNISHI Kouhei Kochi University, Research Institute of Molecular Genetics, Associate Professor, 遺伝子実験施設, 助教授 (50211800)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥15,900,000 (Direct Cost: ¥15,900,000)
Fiscal Year 2005: ¥4,400,000 (Direct Cost: ¥4,400,000)
Fiscal Year 2004: ¥11,500,000 (Direct Cost: ¥11,500,000)
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| Keywords | Ralstonia solanacearum / Bacterial wilt / type III secretion system / hrp / type II secretion system / intercellular spaces / xylem vessels / 青枯病 / 細胞間隙 / 病原-宿主相互作用 / 青枯病-宿主植物相互作用 / タイプIII分泌タンパク質 |
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| Research Abstract |
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.
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