Elucidation of the mechanism underlying delayed mouse oocyte aging by nicotinamide
Project/Area Number |
26450458
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Integrative animal science
|
Research Institution | University of Yamanashi (2015-2016) Kinki University (2014) |
Principal Investigator |
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Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
Keywords | 哺乳類卵子 / 排卵後の老化抑制 / アセチル化修飾 / 卵子の老化 / 代謝 / アセチル化 |
Outline of Final Research Achievements |
In most mammals, without fertilization, the ovulated metaphase II arrested oocytes rapidly lose their developmental potential following ovulation, which is called postovulatory oocyte aging often with characteristic phenotypes such as cytoplasmic fragmentation, abnormal spindle shapes and chromosome misalignments. Accumulating data suggest that many failures in assisted reproduction technologies (ART) are related to oocyte aging. Thus, elucidation of molecular mechanisms underlying oocyte aging and development are important to improve ART. In this study, we addressed how somatic cells impact on oocyte aging after nuclear transfer. Unexpectedly, no acceleration in oocyte aging was observed but distinct phenotypes were found in terms of cytoskeleton. We also examined whether some unknown signals contribute to oocyte aging to find that mTOR signal negatively regulates oocyte aging. Thus, these findings provide new insight for oocyte aging.
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Report
(4 results)
Research Products
(6 results)