2021 Fiscal Year Annual Research Report
Understanding the role of TCP11 and TCP11L3 in hyperactivation
| Project/Area Number |
20K15804
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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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| Keywords | spermatogenesis / flagellum / hyperactivation / sperm motility / mice / cAMP signaling |
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| Outline of Annual Research Achievements |
In this research I knocked out mouse Tcp11L3 using CRISPR/Cas9 and also finished a project on mouse Tcp11. Tcp11L3 is a testis specific gene that is paralogous to Tcp11. Tcp11 is also a testis specific gene that is required for sperm motility that I published in 2020 ( DOI: 10.1093/biolre/ioz226). The molecular function of Tcp11 and Tcp11L3 is unknown, but is thought to function in cAMP signaling. cAMP signaling is required for sperm for sperm motility and hyperactivation. Deletion of mouse Tcp11 resulted in decreased male fertility while deletion of Tcp11L3 alone did not affect male fertility. The decrease in male fertility in Tcp11 knockout male mice was due to decreased sperm motility. Knockout of Tcp11L3 did not affect sperm motility in mice. While Tcp11 knockout mice had reduced male fertility, male Tcp11 knockout mice still sired pups (approximately 1 pup per litter). I hypothesized that Tcp11 knockout mice were capable of producing a small number of pups due to some compensation from Tcp11L3. My future plan is analyze the double knockout of Tcp11 and Tcp11L3 in male mice to determine if Tcp11L3 compensates for the absence of Tcp11.
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Research Products
(1 results)
