2018 Fiscal Year Annual Research Report
Regulation and the role of serine-threonine protein kinase (PBK/TOPK) in spermatogenesis
| Project/Area Number |
17H06799
|
|---|
| Research Institution | Kyoto University |
|---|
Principal Investigator |
ゴエル サンディープ 京都大学, 農学研究科, 特定准教授 (80801745)
|
|---|
| Project Period (FY) |
2017-08-25 – 2019-03-31
|
| Keywords | Testis / Spermatogenesis / Protein Kinase / Gene knockout |
|---|
| Outline of Annual Research Achievements |
Two independent PBK knockout (KO) mouse lines were generated which showed complete loss of PBK protein expression in the testis. Comparative analysis between adult PBK KO and wild-type (WT) mice showed that the testis, epididymis, and seminal vesicle weights did not differ significantly. Histological analysis revealed no significant difference is the tubular diameter. The epididymal sperm number, the percentage of viable sperm, and percentage of morphologically normal sperm did not differ significantly. The mating experiment showed no significant difference in a number of offspring born to WT female that was mated with PBK KO or WT male mice. In-vitro fertilization analysis showed that the fertilization rates of spermatozoa of PBK KO mice and WT mice and the oocyte developmental competence following fertilization were not significantly different. Expression of apoptosis (BAX and BCL2), cell proliferation (PCNA), spermatogonia (UCHL1), spermatogonial stem cell (GFRA1) and meiotic cell (SCP3)-specific proteins were comparable. In conclusion, deletion of PBK gene has no effect on the fertility of male mice. This could be possibly due to compensation of loss of PBK by some other kinase.
|
| Research Progress Status |
平成30年度が最終年度であるため、記入しない。
|
| Strategy for Future Research Activity |
平成30年度が最終年度であるため、記入しない。
|
