2023 Fiscal Year Final Research Report
Elucidation of the role of Rimklb in spermatogenesis.
| Project/Area Number |
20K09633
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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 56040:Obstetrics and gynecology-related
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| Research Institution | Kobe Gakuin 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 | 雄性不妊 / Rimklb / 精子形成 |
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| Outline of Final Research Achievements |
Rimklb is a mammalian homologue of the E. coli enzyme RimK, which catalyzes addition of glutamic acid to the ribosomal protein S6. We generated a Rimklb mutant mouse in which a three-base deletion results in deletion of Ala 29 and substitution of Leu 30 with Val, which we named the RimklbA29del, L30V mutant mouse. RimklbA29del, L30V mutant mice show a decrease in testicular size and weight, and in vitro fertilization demonstrates complete male infertility. Furthermore, we found that a key factor in the mammalian target of the rapamycin/ribosomal protein S6 transcriptional pathway is hyperphosphorylated in the seminiferous tubules of the mutant testis. We conclude that Rimklb has important roles that include spermatogenesis in seminiferous tubules.
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| Free Research Field |
細胞分子生物学
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| Academic Significance and Societal Importance of the Research Achievements |
哺乳動物における生理的役割が分かっていなかったRimklb変異マウスを作製することに成功し、Rimklb変異が精子形成不全、雄性不妊を引き起こすことを明らかにした。学術的にはRimklbが精子形成において重要な役割を果たしていることを初めて示したものである。また、本研究はヒトにおいてもRimklbが精子形成において重要な役割を果たす可能性を示したものであり、男性不妊の原因の一つであるかもしれない。Rimklbの不全をレスキューする方法を見いだすことで、治療法へと繋がる可能性がある。
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