2015 Fiscal Year Final Research Report
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 |
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| Research Field |
Developmental biology
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| Research Institution | Osaka 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 | 母性因子 / 着床前胚 / 初期胚 / 非対称性 / 卵子 |
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| 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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| Free Research Field |
発生生物
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