Regulation of myogenesis via de novo DNA methylation

2020 Fiscal Year Final Research Report

• Project/Area Number: 18K19603
• Research Category: Grant-in-Aid for Challenging Research (Exploratory)
• Allocation Type: Multi-year Fund
• Review Section: Medium-sized Section 56:Surgery related to the biological and sensory functions and related fields
• Research Institution: Tokyo Medical and Dental University
• Principal Investigator: ASAHARA Hiroshi 東京医科歯科大学, 大学院医歯学総合研究科, 教授 (70294460)
• Project Period (FY): 2018-06-29 – 2021-03-31
• Keywords: 筋分化 / DNAメチル化 / DNMT3A / Rp58 / ES細胞

Outline of Final Research Achievements

The muscle differentiation has been a model for developmental and regenerative research since the discovery of the world's first master factor, the transcription factor MyoD. Furthermore, we have reported that the repressive transcription factor Rp58 is a key component of the gene network for muscle differentiation and that DNA methylation is essential for muscle development and regeneration as epigenomic information. On the basis of these findings, the present study clarified the mechanism of cell fate determination involving DNA methylation of Rp58 in muscle differentiation.

Free Research Field

分子生物学、発生・再生医学、整形外科学、リウマチ学

Academic Significance and Societal Importance of the Research Achievements

発生・発達における DNAメチル化は、エピゲノム情報として、細胞の運命を決定するが、その詳細なメカニズムはまだ不明な点がおおい。我々はその鍵を握る遺伝子として、転写抑制因子Rp58とDNAメチル化酵素の相互関係に注目し、筋分化・再生の分子メカニズムの一端を明らかにすることができた。この成果は、今後、筋疾患の病態解明や治療への応用をはじめ、広く、体の恒常性維持、組織再生、発がんなど多くの医学・生物学研究の基盤となることが期待される。