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2023 Fiscal Year Final Research Report

The molecular crosstalk between ZFAT and Geminin in the regulation of hematopoietic stem cell proliferation and differentiation.

Research Project

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Project/Area Number 19K08828
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 54010:Hematology and medical oncology-related
Research InstitutionFukuoka University

Principal Investigator

Yasunaga Shin'ichiro  福岡大学, 医学部, 教授 (50336111)

Co-Investigator(Kenkyū-buntansha) 大野 芳典  福岡大学, 医学部, 講師 (10548986)
白須 直人  福岡大学, 医学部, 講師 (70551422)
Project Period (FY) 2019-04-01 – 2024-03-31
Keywords造血幹細胞 / 自己複製 / 分化 / ZFAT / Geminin / ポリコーム複合体1
Outline of Final Research Achievements

Using a lentivirus vector system, we established a system for the forced expression of ZFAT, a DOX-inducible knockdown system, and a cell-permeable sequence-fused ZFAT recombinant protein introduction system, and confirmed the expression manipulation in hematopoietic stem cells. Additionally, to identify adapter proteins, we used the yeast two-hybrid method to search for ZFAT binding proteins and identified Ring1B, a member of Polycomb Repressive Complex 1 (PRC1). Knockdown experiments of Ring1B indicated abnormalities in chromosome segregation function. These experimental results suggest the possibility of molecular crosstalk between the PRC1-Geminin-Brg1/Smarca4 axis and the ZFAT-BRD4-Brg1/Smarca4 axis.

Free Research Field

幹細胞生物学

Academic Significance and Societal Importance of the Research Achievements

本研究は、造血幹細胞活性を増殖と分化の双方向から支持することを研究代表者が明らかにしたGemininのポリコーム複合体1のE3ユビキチンリガーゼ活性によるタンパク質分解が、造血幹細胞の活性制御に大きな役割を持つ可能性が指摘されているZFATシステムのシグナルを増強し、クロマチンリモデリングを介して染色体分配を促進している可能性を示した。本研究の研究成果は、造血幹細胞を自己複製能と多分化能を維持したままex vivoで増幅する技術開発への分子基盤を提供することが期待される。

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Published: 2025-01-30  

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