Role of maternal Smad2 during early mouse embryo development.
Project/Area Number |
24687028
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Research Category |
Grant-in-Aid for Young Scientists (A)
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Allocation Type | Partial Multi-year Fund |
Research Field |
Developmental biology
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Research Institution | Osaka University |
Principal Investigator |
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Project Period (FY) |
2012-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥27,560,000 (Direct Cost: ¥21,200,000、Indirect Cost: ¥6,360,000)
Fiscal Year 2014: ¥10,660,000 (Direct Cost: ¥8,200,000、Indirect Cost: ¥2,460,000)
Fiscal Year 2013: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2012: ¥11,700,000 (Direct Cost: ¥9,000,000、Indirect Cost: ¥2,700,000)
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Keywords | 母性因子 / 着床前胚 / 初期胚 / 非対称性 / 卵子 / 着床 / 染色体分配 / ヒストン修飾 / 受精 / イメージング / 発生 / 遺伝子 / パターニング / 全能性 / マウス胚 |
Outline of Final Research Achievements |
Early embryogenesis depends on maternal factors present in oocytes. The roles of such factors in embryonic patterning have been well established in Drosophila but remain unclear in mammals. I showed that maternal Nodal signaling is essential for patterning of the mouse pre-implantation embryo. Lack of the Nodal signaling components Foxh1, Smad2, or Nodal in oocytes resulted in loss of toti/pluripotency as well as impaired cell specification before implantation. Genome-wide screening for targets of Nodal signaling in oocytes identified OFT1 and OFT2, the latter of which is implicated in epigenetic regulation. Oocyte-specific deletion of OFT1 or OFT2 recapitulated the defects of the maternal Nodal signaling mutants. My results suggest that epigenetic modification by maternal Nodal signaling regulates toti/pluripotency and cell specification events in the fertilized mouse embryo.
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Report
(5 results)
Research Products
(26 results)