| Project/Area Number |
26860731
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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 |
Hematology
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| Research Institution | Osaka University |
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Principal Investigator |
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| Research Collaborator |
TANAKA Sachiyo 大阪大学, 医学系研究科, 特任研究員
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 造血 / 新規遺伝子 / アポトーシス / コンディショナルノックアウトマウス / 血球発生 / 貧血 / p21 / 血液発生 / 造血幹細胞 |
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| Outline of Final Research Achievements |
Using our previously established homozygous mutant mouse ESC bank, we performed in vitro differentiation screening assays. We identified a previously uncharacterized gene, which we named Ahed, whose null mutant ESCs showed the attenuated production of blood cells during hematopoietic differentiation. This observation was substantiated by hematopoietic cell-specific ablation of Ahed by crossing floxed mice with Vav1-cre transgenic mice, which caused fetal anemia from E14.5 onwards, leading to perinatal lethality. E14.5 fetal liver hematopoietic stem/progenitor cells (LSK cells) from conditional knockout embryos produced less and smaller colonies in a methylcellulose culture.
We found that Ahed encodes a nuclear protein whose loss induces upregulation of the genes involved in apoptosis and cell cycle arrest. Furthermore, Ahed-null E14.5 LSK cells revealed marked apoptosis during culture.
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