Project/Area Number |
20791361
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
Functional basic dentistry
|
Research Institution | Showa University |
Principal Investigator |
YAMADA Atsushi Showa University, 歯学部・口腔生化学教室, 講師 (50407558)
|
Research Collaborator |
KAMIJO Ryutaro 昭和大学, 歯学部・口腔生化学教室, 教授 (70233939)
SUZUKI Dai 昭和大学, 歯学部・口腔生化学教室, 大学院生
|
Project Period (FY) |
2008 – 2009
|
Project Status |
Completed (Fiscal Year 2009)
|
Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2008: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | 遺伝子 / 細胞・組織 / 発生・分化 / シグナル伝達 |
Research Abstract |
To investigate the physiological functions of Rac1, a member of the small Rho GTPase family, we generated Rac1 conditional knockout mice (Rac1 cKO mice) which are characterized by limb bud mesenchyme-specific inactivation of Rac1. Rac1 cKO mice had shorter body length and lower body weight as compared with control mice. Rac1 cKO mice also showed incomplete fusion of the sternum and cranium. The most striking feature of the Rac1 cKO mice fore- and hindlimbs was profound soft tissue syndactyly because of a complete absence of interdigital programmed cell death. Furthermore, the lack of interdigital programmed cell death and associated syndactyly was related to down-regulated gene expression of BMP-2 and BMP-7, which are known to promote apoptosis in the interdigital mesenchyme.
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