| Project/Area Number |
21770232
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Developmental biology
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| Research Institution | Kumamoto University |
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Principal Investigator |
TERABAYASHI Takeshi Kumamoto University, 発生医学研究所・COEリサーチ・アソシエイト (40452429)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2009: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 腎臓発生 / キネシンスーパーファミリー蛋白質 / 細胞骨格 / 微小管 / 細胞接着 / キネシン / 細胞極性 |
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| Research Abstract |
In this study, we performed the functional analysis of Kif26b, a member of kinesin super family proteins. Kif26b is expressed in the metanephric mesenchymes, a population of multipotent kidney progenitors. Disruption of Kif26b causes kidney agenesis because of impaired ureteric bud attraction. In the Kif26b-null metanephros, compact adhesion between mesenchymal cells adjacent to the ureteric buds and the polarized distribution of integrin alpha 8 were impaired, resulting in failed maintenance of Gdnf, a critical ureteric bud attractant. Overexpression of Kif26b in vitro caused increased cell adhesion through interactions with nonmuscle myosin. Thus, Kif26b is essential for kidney development because it regulates the adhesion of mesenchymal cells in contact with ureteric buds.
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