Mechanism of differentiation of fetal Leydig cells by active and suppressive types of nuclear receptors

2018 Fiscal Year Final Research Report

• Project/Area Number: 16H05142
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: General medical chemistry
• Research Institution: Kyushu University
• Principal Investigator: MOROHASHI Ken-ichirou 九州大学, 大学院医学研究院, 主幹教授 (30183114)
• Research Collaborator: Inoue Miki
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: 胎仔精巣 / ライディッヒ細胞 / Ad4BP / Tmsb10 / DHH

Outline of Final Research Achievements

Differentiation of Leydig cells that produce testosterone (androgen) in the testis is regulated by transcription factors such as Ad4BP/SF-1 and growth factors such as DHH. However, the mechanisms for Leydig cell differentiation by these factors remains unclear. In the present study, we newly identified Tmsb10 by a single cell transcriptome study. This factor was demonstrated to work in the process of Leydig cell differentiation from DHH stimulation to enhanced expression of Ad4BP.

Free Research Field

分子生物学

Academic Significance and Societal Importance of the Research Achievements

ライディッヒ細胞の分化に不可欠な転写因子や細胞増殖因子は知られていたが、これらの知見は遺伝子ノックアウトの解析から得られた成果であった。そのため、これらの因子がどのようなメカニズムでライディッヒ細胞を分化させるかは不明であった。本研究は、この点に踏み込むことでライディッヒ細胞の分化メカニズムの理解へ向けた成果となった。