Project/Area Number |
15370092
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Developmental biology
|
Research Institution | Gunma University |
Principal Investigator |
HATADA Izuho Gunma University, Laboratory of Genome Science, Biosignal Genome Resource Center, Department of Molecular and Cellular Biology, Associate Professor, 生体調節研究所, 助教授 (50212147)
|
Co-Investigator(Kenkyū-buntansha) |
HORII Takuro Gunma University, Laboratory of Genome Science, Biosignal Genome Resource Center, Department of Molecular and Cellular Biology, Assistant, 生体調節研究所, 助手 (00361387)
OBATA Yayoi Gunma University, Department of Bioscience, Lecturer, 応用生物科学部, 講師 (70312907)
|
Project Period (FY) |
2003 – 2004
|
Project Status |
Completed (Fiscal Year 2004)
|
Budget Amount *help |
¥15,300,000 (Direct Cost: ¥15,300,000)
Fiscal Year 2004: ¥7,500,000 (Direct Cost: ¥7,500,000)
Fiscal Year 2003: ¥7,800,000 (Direct Cost: ¥7,800,000)
|
Keywords | Methylation / Imprinting / エピジェネティク / 卵母細胞 / ヒストン |
Research Abstract |
DNA methylation plays an important role in transcriptional regulation such as genomic imprinting. Recently histone methylation and RNAi also found to play an important role in transcriptional regulation, however, their relation to DNA methylation has not been clear yet. First we screened the genes whose expression were activated during growth phase of oocyte when imprint was established. We found Dnmt1, Hp1-r, and Epc-1 were activated during this period. Dnmt1 is a DNA methyltransferase and Hp1-r is a binding protein of Suv39HI which is a histoen methylase. Next we examined the relation of RNAi and DNA genome imprinting by using dicer-hypomorphic mouse. As a result, we found ten-fold reduction of dicer is not essential for genomic imprinting.
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