2023 Fiscal Year Final Research Report
Exploring the regulation of sperm fertilization capacity through zinc signaling
| Project/Area Number |
20K06476
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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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| Review Section |
Basic Section 42040:Laboratory animal science-related
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| Research Institution | Kansai Medical University |
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Principal Investigator |
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| Project Period (FY) |
2020-04-01 – 2024-03-31
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| Keywords | 亜鉛 / 受精能獲得 / 精子形成 / 雄性不妊 |
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| Outline of Final Research Achievements |
The purpose of this study was to elucidate the zinc-mediated regulatory mechanism of mammalian fertilization at the molecular level, aiming to understand the causes of infertility, develop treatments, and create contraceptive drugs. To achieve this, we analyzed the function of zinc signaling in reproductive processes by eliminating the zinc transporters expressed in testis. We generated conditional gene-deficient mice of ZnT1, which excretes zinc ions out of cells, and Zip7, a zinc transporter localized on the intracellular organelle membrane of sperm in C. elegans. The deletion of both genes resulted in male sterility, demonstrating their essential role in male reproductive function.
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| Free Research Field |
生殖生物学
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| Academic Significance and Societal Importance of the Research Achievements |
これまでの研究で、亜鉛は精子形成過程や射出後の精子が受精可能な精子へと変化する受精能獲得という現象に重要な制御因子として機能していることが報告されている。しかしながら、これらの亜鉛を介した現象の分子メカニズムは明らかとなっていない。本研究成果により、精巣における亜鉛トランスポーターの機能不全が雄性不妊を引き起こすことが明らかになり、今後さらに詳細な病態解析が行われることによって、不妊症の原因解明・治療や避妊薬の開発に繋がると期待される。
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