2018 Fiscal Year Final Research Report

The role of Pax6 in spermatogenesis and determination of sex bias in the mouse

Research Project

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Project/Area Number	17K19372
Research Category	Grant-in-Aid for Challenging Research (Exploratory)
Allocation Type	Multi-year Fund
Research Field	Biology of Cells to Organisms, and related fields
Research Institution	Tohoku University
Principal Investigator	Osumi Noriko 東北大学, 医学系研究科, 教授 (00220343)
Co-Investigator(Kenkyū-buntansha)	木村龍一東北大学, 医学系研究科, 助教 (00781759)
Research Collaborator	Jasper Germeraad TATEHANA Misako Mai Lingling
Project Period (FY)	2017-06-30 – 2019-03-31
Keywords	Pax6 / 精子形成 / 性比バイアス
Outline of Final Research Achievements	In this study, we examined whether the cause of biased sex ratio observed in spontaneous Pax6 mutant heterozygous (Sey/+) mice is in the process of spermatogenesis. Although the number of spermatogonia in the testis was similar between Sey/+ mice and wild-type littermates, the number of spermatocytes was significantly reduced in Sey/+ mice, suggesting that Pax6 dysfunction may affect the meiotic process. Furthermore, with fluorescent in situ hybridization for X and Y chromosomes, we also analyzed the proportion of sex chromosomes in round spermatids. Surprisingly, it became clear that the proportion of Y chromosome is significantly increased in round spermatids of Sey/+ mice. These results suggest that the biased sex ratio observed in Sey/+ mice may be due to the production of a large proportion of sperm having Y chromosome.
Free Research Field	発生生物学
Academic Significance and Societal Importance of the Research Achievements	出生時の男女比は人種等に関わらずほぼ1.05対1であるが、その理由は不明であった。哺乳類の性は精子の性染色体によって決定され、減数分裂によりXおよびY染色体を持つ配偶子が同じ数だけ産生されるため、仔の性比は理論的には1：1となることが予想され、もし性バイアスが生じるのであれば、なんらかのメカニズムが必要となる。本研究は、減数分裂過程における転写制御因子・クロマチンリモデリング因子Pax6の機能不全が仔の性比に影響することを示した画期的な研究であり、今後その機構を明らかにすることで哺乳類の有する仔の性比調節において、精子形成の制御を介したエピジェネティックな機構が明らかになると期待される。