| Project/Area Number |
16K19566
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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 | Chiba University |
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Principal Investigator |
Mochizuki Makiko 千葉大学, 大学院医学研究院, 特任研究員 (40751300)
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| Research Collaborator |
IWAMA Atsushi
URA Kiyoe
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | Mmset / Whsc1 / Nsd1 / HSC / H3K36me2/3 / Nsd2 / FA / MMSET / ヒストン修飾 / 造血幹細胞 / 分化 / DNAダメージ修復 |
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| Outline of Final Research Achievements |
Wolf-Hirschhorn syndrome candidate 1 (WHSC1), also known as NSD2 or MMSET, functions as a one of the Histone H3 Lysin36 methyltransferase (H3K36me) transcriptional regulation together with developmental transcription factors and that the Whsc1 deficiency is responsible for WHS.
In this reserch, we showed that Whsc1 is required for normal Hematopoietic stem cell (HSC) homeostasis. We performed Hematopoietic analysis in both Whsc1 conventional knockout (KO) and conditional knockout (cKO) mice. HSC number was slightly increased in adult Whsc1 cKO. Nevertheless competitive reconstitution of hematopoietic cell analysis reveals that Whsc1-deficient HSCs impaired reconstitution capacity in vivo. These data indicate DNA damage repair associated modification H3K36me plays important role for HSC self-renewal, differentiation and reconstitution.
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