| Project/Area Number |
17K15392
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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 |
Integrative animal science
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2017: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 減数分裂 / HORMAD1相互作用因子 / 細胞・組織 / 遺伝学 |
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| Outline of Final Research Achievements |
Gametes such as sperm and egg are produced through a specialized cell divisions called meiosis. During this process, homologous chromosomes pair and exchange part of their genetic information by homologous recombination. It is know that there is a mechanism which monitor if homologous chromosomes pair correctly. However, it has been elusive how factors responsible for this mechanism, such as HORMAD1, are recruited to where chromosomes pair. In this study, it was revealed that meiotic cohesin proteins play a key role in recruitment of HORMAD1 to the chromosome axis.
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| Academic Significance and Societal Importance of the Research Achievements |
今回の成果はマウスを用いて検証されたが、ヒトの生殖細胞でも同じくコヒーシンやHORMAD1タンパク質が働いている。この仕組みが正常に働かなければ減数分裂組換え反応がうまく起こらなくなるため、精子・卵子形成が著しく低下し不妊となってしまう。ヒトの不妊症は原因が不明とされる症例が多いことが知られているため、今回の発見は、卵子・精子形成不全を示す不妊症の病態の解明に資することが期待される。
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