| Project/Area Number |
24592813
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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 |
Functional basic dentistry
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| Research Institution | Showa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KAMIJO Ryutaro 昭和大学歯学部, 口腔生化学教室, 教授 (70233939)
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| Co-Investigator(Renkei-kenkyūsha) |
AIBA Atsu 東京大学大学院医学系研究科, 附属疾患生命工学センター研究基盤部門・動物資源研究領域, 教授 (20271116)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | コンディショナルノックアウトマウス / 発生学 / 軟骨 / 遺伝子改変マウス / シグナル伝達 |
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| Outline of Final Research Achievements |
Rac1 and Cdc42 are Rho small GTPases known to regulate multiple cellular functions, including cytoskeletal organization, proliferation, and apoptosis. Recently, their tissue-specific roles have been revealed, especially in mammalian limb development, using limb bud mesenchyme-specific inactivated Rac1 (Rac1fl/fl; Prx1-Cre; Rac1 cKO) and Cdc42 (Cdc421fl/fl; Prx1-Cre; Cdc42 cKO) conditional knockout mice. Both strains demonstrate striking syndactyly of the fore- and hindlimbs. That in Rac1 cKO mice is caused by a failure of interdigital programmed cell death, while syndactyly in Cdc42 cKO mice is caused by not only a failure of interdigital programmed cell death, but also fusion of metacarpals. Also, most of the Cdc42 cKO neonates were viable at birth, though they appeared weaker and no milk was found in their stomachs, and died within a few days. In the present study, we analyzed mechanisms of Rac1 and Cdc42 functions in bone and cartilage formation.
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