| Project/Area Number |
24790198
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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 anatomy (including Histology/Embryology)
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| Research Institution | Japan Aerospace Exploration Agency (2013)
Kyoto Prefectural University of Medicine (2012) |
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Principal Investigator |
SHIBA DAI 独立行政法人宇宙航空研究開発機構, 有人宇宙ミッション本部, 主任研究員 (50360722)
|
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 一次繊毛 / 腎臓 / 嚢胞 / メカノストレス / 前庭機能 / シグナル伝達 / 繊毛 / 分子構造 / 生体応答 / 核移行 |
|---|
| Research Abstract |
Primary cilia have diverse functions in cell signaling pathways, including mechanosensation and hedgehog signaling. More than 1000 proteins are now identified to localize in the cilium. Nephronophthisis (NPHP) is an autosomal recessive cystic kidney disease. Among 12 reported Nphp gene products, Inv/Nphp2 and Nek8/Nphp9 are localized to the proximal segment in the primary cilium. However, the functional relationships are unknown. This study focused on phenotype analysis of nek8 knockdown embryos and the genetic relationship between nek8 and inv in zebrafish. Knockdown of nek8 produced pronephric cysts. Simultaneous knockdown of nek8 and inv synergistically increased the incidence of these defects. Interestingly, nek8 mRNA rescued inv morphant phenotypes, although inv mRNA could not rescue nek8 morphant phenotypes. These results suggest that Nek8 acts downstream of Inv function.
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