| Project/Area Number |
25430085
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Laboratory animal science
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| Research Institution | Kyoto University (2014-2015)
Kanazawa University (2013) |
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Principal Investigator |
Naruse Chie 京都大学, 医学(系)研究科(研究院), 助教 (30372486)
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| Co-Investigator(Kenkyū-buntansha) |
ASANO Masahide 京都大学, 大学院医学研究科, 教授 (50251450)
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| Co-Investigator(Renkei-kenkyūsha) |
SUGIHARA Kazushi 京都大学, 大学院医学研究科, 技術職員 (10377418)
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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 |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | マウス / 脱メチル化酵素 / ホメオティック変異 / ヒストン脱メチル化 / HP1 / 神経幹細胞 / エピジェネティクス / 発生 / 神経 / Hox遺伝子 |
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| Outline of Final Research Achievements |
HP1gamma mutant neurospheres had tendency to differentiate into neurons and astrocytes, and not only H3K9 but H3K27 methylation decreased in HP1gamma mutant neurospheres. Jmjd3 and Utx are H3K27 demethylases and thought to be involved in the many human diseases, however, the functional differences between Jmjd3 and Utx in mammals are still unclear. We examined both Jmjd3 and Utx deficient embryos. The results suggest that Jmjd3, but not Utx is involved in the axial patterning through Hox regulation in mice in contrast to previous reports that not Jmjd3 but Utx determines the axis formation via Hox regulation in zebrafish and nematode. Furthermore, Jmjd3 mouse mutants lacking only demethylase activity were examined since Jmjd3 functions in two ways: demethylase-dependent and independent. They showed the same phenotypes as Jmjd3 deficient embryos, suggesting that demethylase activity of Jmjd3 is crucial for the axial patterning in mice.
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