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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| Project Status |
Completed (Fiscal Year 2015)
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| 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 |
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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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Report
(5 results)
Research Products
(25 results)
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[Journal Article] Fluid flow and interlinked feedback loops establish left-right asymmetric decay of Cerl2 mRNA in the mouse embryo2012
Author(s)
Nakamura, T., Saito, D., Kawasumi, A., Shinohara, K., Asai, Y., Takaoka, K., Dong, F., Takamatsu, A., Belo, J.A., Mochizuki, A., and Hamada, H.
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Journal Title
Nat.Communic
Volume: 3
Issue: 1
Pages: 1322-1322
DOI
Related Report
Peer Reviewed
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