Understanding the "genome adaptation" in fertilized embryo

2014 Fiscal Year Final Research Report

• Project Area: Systematic study of chromosome adaptation
• Project/Area Number: 22125007
• Research Category: Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
• Allocation Type: Single-year Grants
• Review Section: Biological Sciences
• Research Institution: The University of Tokyo
• Principal Investigator: OKADA Yuki 東京大学, 分子細胞生物学研究所, 准教授 (60546430)
• Co-Investigator(Renkei-kenkyūsha): SHIRAHIGE Katsuhiko 東京大学, 分子細胞生物学研究所, 教授 (90273854) ; SHIRAHIGE Katsuhiko 東京工業大学, 大学院・生命理工学研究科, 教授 (90501106) ; MAKINO Katsuhiko 東京大学, 分子細胞生物学研究所, 特任助教 (60431334) ; PARK Sung-Joon 東京大学, 医科学研究所, 特任講師
• Research Collaborator: AOSHIMA Keisuke ; HADA Masashi
• Project Period (FY): 2010-04-01 – 2015-03-31
• Keywords: 発生生物学 / ゲノム / エピゲノム / リモデリング / クロマチンダイナミクス

Outline of Final Research Achievements

In this study, we aimed i) the establishment of ChIP-seq from very small number of cells, especially mouse preimplantation embyors, and ii) analysis of the (epi)genome reprogramming in fertilized 1-cell embryos using the new ChIP-seq technology.
In the former project, we obtained substantial improvement of reproducibility in top ~15% sequence reads by modifying the step of linear amplification of sequence libraries, although further modifications are still required to reach the goal. In the latter project, instead of using the new ChIP-seq method, we utilized recently identified histone mutants, which erase endogenous histone methylations at the mutated sites, to investigate the importance of histone methylations in preimplantation embryos. As a result, we identified that paternal-specific H3K4 monomethylation by Mll3/4 is required for transcription of paternal genome in late 1-cell embryos, likely through enhancer activation.

Free Research Field

エピゲノム