| Project/Area Number |
15K07778
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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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| Research Field |
Integrative animal science
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| Research Institution | Shizuoka University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
藤井 渉 東京大学, 大学院農学生命科学研究科(農学部), 助教 (40708161)
伊藤 千鶴 千葉大学, 大学院医学研究院, 講師 (80347054)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 精子形成 / 不妊 / マウス / 受精能獲得 / Slc22a14 / Dlec1 / SLCトランスポーター / 精子 / アンドロロジー / 生殖細胞 / ノックアウトマウス / ゲノム編集 / ノックアウト |
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| Outline of Final Research Achievements |
We investigated expression profile and physiological role of Slc22a14 and Dlec1 in mice，and found that these genes play a crucial role for male fertility. For example, Slc22a14 is expressed specifically in sperm, and if this gene was disrupted, motility and fertilizing ability of sperm were significantly decreased and thus reproductive ability were markedly impaired. In addition, we found that Dlec1-deficient male mice are completely infertile. Sperm differentiation was abnormal and almost no sperm were seen in cauda epididymis in Dlec1-deficirnt mice. Since Slc22a14 and Dlec1 are conserved in humans, above results suggest that these genes are candidate causative genes of human male infertility.
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