| Project/Area Number |
15K19003
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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 |
General medical chemistry
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2015-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | MAPK / SAPK / PLK4 / 中心体 / 染色体不安定性 / 小頭症 / MAPキナーゼ / ストレス応答MAPK / リン酸化 / 細胞周期 |
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| Outline of Final Research Achievements |
Centrosomes function as bipolar spindles, which are essential for equal chromosome segregation. Therefore centrosome duplication is strictly regulated to once per cell cycle. Even under stress condition, centrosome number is maintained in normal cells. However, the molecular mechanism had remained unclear. We have reported that p53 and SAPK pathways cooperatively regulate PLK4-diriven centrosome duplication under stress, thereby maintaining the numeral integrity of centrosomes. This time we identified the novel target of SAPK in centrosome duplication arrest. Moreover we tried to elucidate the mechanism by which PLK4 translocalizes to mother centrioles.
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