| Project/Area Number |
16K14892
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Applied microbiology
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| Research Institution | Tokyo University of Agriculture |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | メチローム / シトシンメチル化 / 挿入配列 / トランスポゼース / アデニンメチル化 / 親鎖識別機構 / 胞子形成 / 誤対合修復 / 実験進化 / 分子シャペロン / 遺伝子発現 / 進化 |
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| Outline of Final Research Achievements |
In terms of maintenance mechanisms of genome structure, we focused on two phenomena, methylation and IS transposition. Bacterial epigenetics has been noted only recently and correlation with growth regulation is totally unknown. In this study, we demonstrated sporulation specific methylation in Bacillus subtilis. While transposition of IS derived from natto strain has been found to be strictly dependent on recA gene, its essential function on IS transposition was not homologous recombination but ATP hydrolysis activity. In addition, we explored the possible evolutionary background of the unique feature of 168 genome which harbored no IS element. Successive culture of 168 cells with our newly developed IS transposition assay system revealed that 168 cells allowed IS transposition to some extent, but later inhibitory effect of IS transposition seemed to emerge by inactivating transposase activity. Those transposition-capable cells grew slowly and would be titrate out during evolution.
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