2013 Fiscal Year Final Research Report
Identification of regulatory molecules governing self-renewal versus differentiation of spermatogonial stem cells
| Project/Area Number |
23380168
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Applied animal science
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| Research Institution | Kitasato University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
垣内 一恵 北里大学, 獣医学部, 助教 (90509184)
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Keywords | 生殖幹細胞 / 精原幹細胞 / 精子形成 / 自己複製 |
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| Outline of Final Research Achievements |
Comparative gene expression analysis between differentiation-deficient spermatogonial stem cells (SSCs) and wild-type SSCs indicated that the KIT expression involves in maintaining an undifferentiated state of SSCs. Factor X was identified as one of the genes that were down-regulated in differentiation-deficient SSCs. Factor X expression was restricted in undifferentiated spermatogonia including SSCs in murine testes. Down regulation of Factor X in cultured SSCs induced differentiation. On the other hand, when Factor X was over-expressed in cultured SSCs, their self-renewing proliferation was dramatically impaired. These results suggest that Factor X, which was identified in this study, is a regulatory molecule governing self-renewal and differentiation of murine SSCs.
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| Free Research Field |
幹細胞生物学
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| Academic Significance and Societal Importance of the Research Achievements |
本研究課題において、精原幹細胞の自己複製と分化を制御する新たな因子として因子Xが同定された。これまで発現量の低下により分化を誘導する因子は複数同定されているが、過剰発現により自己複製増殖を阻害する因子は同定されていない。因子Xの過剰発現による自己複製増殖の阻害は休止状態への移行である可能性がある。組織内で最も未熟な幹細胞は休止状態にあるため、因子Xの発現がそうした休止状態への移行に関与している可能性について検証することは重要である。今後の課題は、因子Xがいかに精原幹細胞の自己複製増殖と分化誘導を制御しているかを明らかにすることである。
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Research Products
(7 results)
