| Project/Area Number |
15K07080
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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 |
Developmental biology
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| Research Institution | Kumamoto Health Science University |
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Principal Investigator |
Tanaka Satomi 熊本保健科学大学, 保健科学部, 教授 (10321944)
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| Project Period (FY) |
2015-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 生殖細胞 / マウス / Six1 / Six4 / 生殖腺 / 性分化 / 卵巣 / 顆粒膜細胞 |
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| Outline of Final Research Achievements |
In mice, BMP and WNT signaling activities play essential roles in primordial germ cell (PGC) formation through the substantial upregulation of Prdm1 (Blimp1) in PGC precursor cells, but their precise mechanisms remain elusive. We found that the transcription factors Six1 and Six4 are required for PGC formation at the downstream to BMP and WNT signaling pathways. Loss of Six1 and Six4, but neither alone, resulted in a reduction in number of PGCs accompanied by the failure of the substantial Prdm1 upregulation in PGC precursors. Further, we identified Prdm1 as a downstream target of Six1/Six4, and Six1/Six4 are the reportedly target genes of Prdm1. These findings suggest that together with T the Prdm1-Six1/Six4 transcriptional positive-feedback loop may contribute to the substantial Prdm1 upregulation during PGC formation.
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| Academic Significance and Societal Importance of the Research Achievements |
マウスの胎仔卵巣を構成する２つの細胞系譜である生殖細胞と生殖腺体細胞は、その細胞数比が生殖細胞分化に大きな影響を与えるが、その形成を共通して制御する分子機構については知られていなかった。本研究により、転写因子Six1とSix4が、異なる発生段階と胚体内の場所で、それぞれの前駆細胞形成を制御するユニークな分子機構が明らかとなった。
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