| Project/Area Number |
26840060
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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 |
Cell biology
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| Research Institution | Tohoku University |
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Principal Investigator |
Nagai Tomoaki 東北大学, 生命科学研究科, 助教 (10723059)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 分裂期紡錘体 / Furry / 微小管 / 体細胞分裂 / 劣性遺伝性精神遅滞 / 分裂期紡錘体形成 / CCT複合体 / 紡錘体微小管 |
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| Outline of Final Research Achievements |
Furry (Fry) is a large protein that is evolutionarily conserved from yeast to human. Fry and its orthologues are implicated in the control of cell growth and morphogenesis. Mammalian Fry is essential for the formation of mitotic spindle. In this study, we investigated the role of Fry in the formation of mitotic spindle and identified CCT complex and Sav1 as novel Fry-binding proteins. Although Fry directly binds to CCT, it is not involved in the regulation of folding activity of CCT. We also investigated the role of Fry mutant (R1197X), which is the causal mutation in recessive mental retardation. This mutant (N-1196) cannot bind to Plk1, an essential kinase for the formation of bipolar mitotic spindle, due to lack of C-terminal binding region of Fry. Moreover, although Fry binds to microtubules and NDR via its N-terminal region, Fry N-1196 cannot bind to them. These results suggest that Fry R1197X mutation lacks the specific function of its wild-type.
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