| Project/Area Number |
17K08828
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Bacteriology (including mycology)
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| Research Institution | Osaka University |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 腸炎ビブリオ / 3型分泌装置 / 発現制御 / ３型分泌装置 / 細菌 |
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| Outline of Final Research Achievements |
Vibrio parahaemolyticus is a leading cause of seafood-borne bacterial gastroenteritis. Major virulence factors of V. parahaemolyticus are two type III secretion systems whose gene expression is affected by external conditions. In this study, we determined that VtrA, a T3SS2 master regulator, is a membrane-bound regulator. We also showed that bile, a host-derived activator of VtrA, induces the oligomerization of VtrA. Engineered oligomerization of VtrA conferred transcriptional regulatory activity and a greater affinity for the promoter region of its target gene vtrB. These findings propose that VtrA oligomerizes in response to bile, which may facilitate its binding the target DNA, thus enhancing its transcriptional regulatory activity. Also, we identified a gene that is required for the environmental regulation of T3SS2 gene expression.
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| Academic Significance and Societal Importance of the Research Achievements |
病原細菌は感染時の宿主内環境を感知し、感染に必要な病原因子を的確に発現させることで病原性を発揮していると考えられている。一方で腸炎ビブリオの病原性メカニズムの研究動向はその病原因子であるT3SSの作用の解析が主となり、その発現制御に対する理解は乏しい状況にあった。これに対し本研究成果は腸炎ビブリオの感染時の外的環境変化に応答した病原因子の発現制御の分子メカニズムの一端を解明し、腸炎ビブリオの病原性メカニズムの全体像の理解を進展せしむるものと考えらえる。
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