| Project/Area Number |
25870116
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Bacteriology (including mycology)
Functional biochemistry
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| Research Institution | Gunma University |
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Principal Investigator |
KURUSHIMA Jun 群馬大学, 医学(系)研究科(研究院), 助教 (50636488)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 腸球菌 / 溶菌酵素 / 細胞壁 / 細胞分裂 / プラスミド / Enterococcus faecalis / ペプチドグリカン / 臨床分離株 / 質量分析 / 蛍光イメージング / 細菌間相互作用 / バクテリオシン / 抗菌タンパク質 / ペプチドグリカン分解酵素 |
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| Outline of Final Research Achievements |
We investigated the molecular mechanism underlying the bacteriolytic activity of bacteriocin Bac41 that is produced by Enterococcus faecalis clinical isolate. BacL1 protein, which is an essential secreted component of Bac41, showed a cell wall degrading activity against E. faecalis peptidoglycan, and binds to cell dividing-associated region of the target E. faecalis cell surface to lead bacteriolysis. By contrast, neither the binding of BacL1 nor the bacteriolysis was observed in the static E. faecalis cells. The binding of BacL1 was specifically detected in L-Ala-L-Ala crossbridged peptidoglycan but not in peptidoglycan with other crossbridge structure, potentially explaining narrow antimicrobial spectrum of Bac41.
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