2015 Fiscal Year Final Research Report
The molecular endocrinology analysis of early fertility decline mouse to develop the novel breeding marker of livestock animals
| Project/Area Number |
24688028
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Partial Multi-year Fund |
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| Research Field |
Applied animal science
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| Research Institution | Hiroshima University |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2016-03-31
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| Keywords | 生殖 / 受精 / 卵巣 / 精巣 |
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| Outline of Final Research Achievements |
In this study, we developed granulosa cell/leydig cell specific Nrg1 mutant mice to understand the roles of NRG1 in reproductive organs. In female, The expressed NRG1 by granulosa cells acts on cumulus cells to down-regulate Ca2+ induction. The regulation is important for not only the induction of gene expression but also the control of cell-cell communication. Both regulatory systems by NRG1 are involved in the timing of oocyte maturation and induction of ovulation. The synchronization induces to adjust the best timing of fertilization to the timing just after ovulation. In male mice, NRG1 is expressed in leydig cells of infant testis. The expression is essential for the proliferation of the cells, which predicts the ability to produce androgen in adult testis. The hyper production of androgen is required for spermatogenesis and sexual behavior.
Therefore, we concluded that NRG1 is important factors in both female and male to make a full activity of reproductive organs.
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| Free Research Field |
動物生産科学
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