| Project/Area Number |
25293345
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Keio University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
AKUTSU HIDENORI 国立成育医療研究センター, 生殖・細胞医療研究部, 部長 (50347225)
HATA KENICHIRO 国立成育医療研究センター, 周産期病態研究部, 部長 (60360335)
TSUMURA HIDEKI 国立成育医療研究センター, 実験動物管理室, 室長 (20180052)
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| Co-Investigator(Renkei-kenkyūsha) |
UMEZAWA AKIHIRO 国立成育医療研究センター, 生殖・細胞医療研究部, 部長 (70213486)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥17,810,000 (Direct Cost: ¥13,700,000、Indirect Cost: ¥4,110,000)
Fiscal Year 2015: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2014: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2013: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
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| Keywords | 生殖医学 / 着床前期胚 / 遺伝子発現パターン / ZGA / 新規遺伝子 / SCAN / 染色体ギャップ / 発現プロファイリング / ゲノム不安定性 / MEP50 |
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| Outline of Final Research Achievements |
This study found novel mouse genes (e.g. Kzpi encoding KRAB zinc-finger and Zfpi encoding SCAN-zinc finger) exclusively and zygotically expressed in preimplantation embryos and ES cells. Kzpi-deficient mice showed smaller litter sizes. Interestingly, most imprinted genes were down regulated and the methylation levels of differentially methylated regions (DMRs) were decreased in homozygous ES cells. Kzpi was thus suggested to maintain DMRs against genome-wide demethylation in preimplantation embryos. However, transgenerational phenotypic attenuation of Kzpi-deficient mice was observed: normal methylation patterns of DMRs in Kzpi-deficient blastocyst and ES cells. Zfpi-deficient mice did not show any phenotype, but karyotype analysis revealed chromosomal gaps. Kzpi-deficient ES cells generated a teratoma composed of all the three-germ layer, but gave rise to embryonal carcinoma.
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