Uncovering the regulatory mechanism of meiotic entry in mammalian germ cells

2023 Fiscal Year Final Research Report

• Project/Area Number: 21K06843
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 48040:Medical biochemistry-related
• Research Institution: Saitama Medical University
• Principal Investigator: Suzuki Ayumu 埼玉医科大学, 医学部, 講師 (80639708)
• Co-Investigator(Kenkyū-buntansha): 奥田 晶彦 埼玉医科大学, 医学部, 教授 (60201993)
• Project Period (FY): 2021-04-01 – 2024-03-31
• Keywords: Max / PRC1.6 / Myc / 減数分裂 / 生殖細胞

Outline of Final Research Achievements

This study focused on the PRC1.6 complex, which includes MAX, and its role in regulating the transition from mitosis to meiosis in germ cells. We demonstrated that germ cell-specific knockout of MAX induces meiosis in both male and female primordial germ cells before sexual differentiation and found that MAX protein levels decrease significantly prior to meiotic initiation.
We worked on elucidating the control mechanism of meiotic initiation by MYC/MAX and MGA/MAX (PRC1.6) complexes, identifying a genomic region (MUR) involved in MAX expression regulation. These findings contribute to our understanding of the molecular basis of the mitosis-to-meiosis transition in germ cells and are expected to help clarify the causes of reproductive disorders. In the future, we aim to further elucidate the mechanisms of meiotic initiation and its disruption.

Free Research Field

発生生物学、幹細胞生物学

Academic Significance and Societal Importance of the Research Achievements

本研究は、MAXによる減数分裂遺伝子の抑制メカニズムの解明を通して、生殖細胞の運命決定や配偶子形成の基礎的理解を深めることを目的としている。この研究により、減数分裂開始の分子基盤が明らかになれば、体外での配偶子作成技術の向上や不妊症の新たな治療法の開発につながることが期待される。さらに近年、減数分裂遺伝子が腫瘍の発生や悪性化に関与していることが報告されているため、生体内での減数分裂遺伝子の抑制機構の理解は、がんの発生・悪性化のメカニズム解明にも役立つと考えられる。したがって将来的には、がんの予防法や治療法の進歩にも貢献できる可能性がある。