| Project/Area Number |
20K15804
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 44020:Developmental biology-related
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| Research Institution | Osaka University |
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Principal Investigator |
Castaneda Julio 大阪大学, 微生物病研究所, 特任助教(常勤) (00791659)
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| Project Period (FY) |
2020-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2021: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2020: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | sperm / sperm motility / infertility / Tcp11 / cAMP signaling / spermatogenesis / flagellum / hyperactivation / mice / cAMP |
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| Outline of Research at the Start |
This research plan will examine the role of two genes thought to be important for the production of healthy sperm. Using the mouse as a model, I will determine if these two genes help in producing functional sperm and the manner in which these two genes carry out this function.
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| Outline of Final Research Achievements |
This research identified one gene (Tcp11) that is important for sperm motility, and a related gene (Tcp11 Like 3) that is not necessary for sperm movement. When we remove the Tcp11 gene in mice, sperm have decreased movement and the male mice are infertile. Humans also have the Tcp11 gene, and this research suggests that Tcp11 may also be important for sperm motility in men.
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| Academic Significance and Societal Importance of the Research Achievements |
This research identified Tcp11 as important for sperm motility. The research suggests that Tcp11 is functioning through the cAMP signaling pathway. The societal benefits is in human reproduction. In infertile men whose sperm are immotile, we think Tcp11 might be the cause of this defect.
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