Elucidation of molecular mechanism for base excision repair pathway-mediated active demethylation by PRDM14

2015 Fiscal Year Final Research Report

• Project/Area Number: 24681040
• Research Category: Grant-in-Aid for Young Scientists (A)
• Allocation Type: Partial Multi-year Fund
• Research Field: Genome biology
• Research Institution: Kwansei Gakuin University
• Principal Investigator: Seki Yoshiyuki 関西学院大学, 理工学部, 准教授 (20435655)
• Project Period (FY): 2012-04-01 – 2016-03-31
• Keywords: 多能性幹細胞 / 初期化 / 生殖細胞 / 再生医学

Outline of Final Research Achievements

Germline cells are sole source of next generation in multicellular organism, which is called cellular totipoency. Germ cells erase genome-wide DNA methylation and histone modifications to acquire cellular totipotency during their development.
In this study, we have tried to identify the molecular mechanisms and biological significance of base excision repair-mediated active demethyaltion by PRDM14. We have shown that PRDM14 regulates the activity of TET proteins to promotes active DNA demethylation in embryonic stem cells (ESCs). We have further demonstrated that PRDM14 converts epiblast-like cells (EpiLCs) to ESCs mediated by the enhancement of OCT3/4-binding at target locus through active DNA demethylation.

Free Research Field

エピジェネティクス