A novel regulatory mechanism of planar polarity via the third group of PCP factors
| Project/Area Number |
16H04791
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Developmental biology
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| Research Institution | Akita University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
秋山 正和 北海道大学, 電子科学研究所, 助教 (10583908)
鮎川 友紀 秋田大学, 医学系研究科, 助教 (80586165)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
Fiscal Year 2018: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2016: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
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| Keywords | 平面内細胞極性 / PCP / ショウジョウバエ / 発生・分化 / 細胞・組織 / 極性 |
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| Outline of Final Research Achievements |
Planar cell polarity (PCP) is the collective alignment of polarized cells within the plane of the epithelium. We previously carried out a genome-wide RNAi screen using the Drosophila notum and identified novel genes involved in multiple developmental processes including PCP. One PCP gene we identified in the RNAi screen is jitterbug (jbug), which is the Drosophila filamin ortholog. However, the molecular mechanism by which Jbug regulates PCP remains unclear. In this study, using fly genetics and live imaging techniques, we elucidated a mechanism underlying PCP defects induced by loss of function of Jbug.
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| Academic Significance and Societal Importance of the Research Achievements |
平面内細胞極性（PCP）とは、組織平面において細胞や毛などの付属器の向きが特定の方向に揃う現象であり、組織・器官の機能発現に重要な役割を果たす。近年、PCP制御系が、膵β細胞の分化や嚢胞腎などに関わることが報告されるとともに、ヒトPCP遺伝子の変異により二分脊椎や僧帽弁逸脱が惹起されることも認知されている。本研究の成果は、組織構築機構の理解のみならず、創薬や医療基盤の創成に資する知見を提供できるものと考えている。
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Report
(4 results)
Research Products
(16 results)
