Study on epigenetic regulation of Nodal gene
| Project/Area Number |
25850219
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Integrative animal science
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| Research Institution | Waseda University |
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Principal Investigator |
Arai Daisuke 早稲田大学, 理工学術院, 講師 (20624951)
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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 |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | Nodal / エピジェネティクス / ヒストン修飾 / 細胞分化 / がん / ノンコーディングRNA / DNAメチル化 / クロマチン / 胚性幹細胞 |
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| Outline of Final Research Achievements |
Nodal gene plays essential roles in embryonic development. Meanwhile, expression of Nodal gene is strictly repressed in adults, and reactivation of Nodal gene is thought to contribute to malignant transformation. In this project, we investigated mechanisms for regulation of Nodal gene in terms of epigenetics. We found a region exhibiting dynamic changes in DNA methylation at upstream of transcriptional start site of mouse Nodal gene. This region, termed ERE, was a novel regulatory element that induced expression of Nodal in mouse embryonic stem cells. We confirmed that trimethylation of histone H3 lysine 27 (H3K27me3) at ERE was required for transcriptional repression of Nodal gene in differentiated cells. Furthermore, ERE is conserved in human genome, and H3K27me3 was decreased at ERE in human cancer cells.
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Report
(4 results)
Research Products
(5 results)
