| Project/Area Number |
20590330
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Human genetics
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| Research Institution | Saga University |
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Principal Investigator |
SOEJIMA Hidenobu Saga University, 医学部, 教授 (30304885)
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| Co-Investigator(Kenkyū-buntansha) |
JOH Keiichiro 佐賀大学, 医学部, 准教授 (90124809)
HIGASHIMOTO Ken 佐賀大学, 医学部, 助教 (30346887)
KUGOH Hiroyuki 鳥取大学, 大学院・医学系研究科, 准教授 (40225131)
KOSEKI Haruhiko 理化学研究所, 免疫器官形成研究グループ・グループディレクター (40225446)
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| Research Collaborator |
YATSUKI Hitomi 佐賀大学, 医学部, 技術専門職員
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2008: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | エピジェネティクス / ゲノム刷り込み / 刷り込みドメイン / non-coding RNA / siRNAライブラリー / KIP2 / LIT1刷り込みドメイン |
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| Research Abstract |
The aim of this study is to clarify regulatory mechanisms of the imprinting. (1) To distinguish imprinting disrupted cells from normal cells by expression of marker genes, Igf2r was targeted with YFP cassette on the maternal allele in F1ES cell. We are trying to introduce Igf2r-2A-E2Crimsoncassette into the paternal allele. The cells will be screened with siRNA library to identify regulatory factors for the imprinting. (2) non-coding RNA LIT] would recruit HDAC(s) to the promoter region of KvLQTl to deacetylate histone H3 and to make heterochromatin, leading to repress the KvLQTl gene on the paternal chromosome. (3) At mouse Commdl/U2af1-rsl imprinted domain, that interference with paternal Commdl transcription by the oppositely directed U2afl-rs1 transcription seemed to be a mechanism for the maternal predominantly expression of Commdl gene.
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