Regulatory mechanism on the development of primordial germ cells and the mechanism of tumor development due to its disruption

2020 Fiscal Year Final Research Report

• Project/Area Number: 17H05046
• Research Category: Grant-in-Aid for Young Scientists (A)
• Allocation Type: Single-year Grants
• Research Field: Integrative animal science
• Research Institution: Yokohama National University
• Principal Investigator: Suzuki Atsushi 横浜国立大学, 大学院工学研究院, 准教授 (60467058)
• Project Period (FY): 2017-04-01 – 2021-03-31
• Keywords: 精巣テラトーマ / 精原細胞

Outline of Final Research Achievements

Mouse primordial germ cells occasionally deviate from the differentiation pathway to sperm and convert into pluripotent cells in the seminiferous tubules, and then variously differentiate to form teratomas. However, the molecular mechanism by which such a phenomenon occurs in vivo is still unknown. We found that a deficiency of the RNA-binding protein Dead end 1 induces the development of testicular teratoma in 129 strain mice. On the other hand, the deficiency of Dead end 1 in the postnatal spermatogenesis process did not cause the development of testicular teratomas and caused a decrease in spermatogonia. From the above, it was shown that the function of Dead end 1 in primordial germ cells is involved in the onset of testis teratoma.

Free Research Field

動物生命科学

Academic Significance and Societal Importance of the Research Achievements

本件研究はマウス始原生殖細胞特異的に発現するRNA結合タンパク質Dead end1とその結合タンパク質の欠損が、129系統マウスにおいて精巣テラトーマを高確率で発症することを示した。これは、始原生殖細胞の発生を制御するRNA分子機構の破綻が腫瘍発生の引き金となることを示しており、今後、Dead end1の分子機能を明らかにすることで腫瘍発生の分子機構が明らかになる可能性がある。また、ヒトの精巣腫瘍とマウス精巣テラトーマは共通の遺伝子が原因となることがあることから、マウス精巣テラトーマ発症の分子機構の解明はヒト精巣腫瘍発症の分子機構解明へとつながる可能性がある。