- 著者
- Makoto Tachibana
- 出版者
- The University of Tokushima Faculty of Medicine
- 雑誌
- The Journal of Medical Investigation (ISSN:13431420)
- 巻号頁・発行日
- vol.62, no.1.2, pp.19-23, 2015 (Released:2015-03-27)
- 参考文献数
- 47
- 被引用文献数
- 12 14
Epigenetics is the study of changes in gene function that cannot be explained by changes in DNA sequence. A mammalian body contains more than two-hundred different types of cells, all derived from a single fertilized egg. Epigenetic gene regulation mechanisms essentially contribute to various processes of mammalian development. The essence of epigenetic regulation is the modulation of gene activity through changes in chromatin structure. DNA methylation and histone modifications are the major epigenetic mechanisms. Sex determination is the process of establishing a gender. Sry, the sex-determining gene in therian mammals, initiates testis differentiation. Recent studies have provided evidence that epigenetic mechanisms contribute to Sry regulation. J. Med. Invest. 62: 19-23, February, 2015
1 0 0 0 OA Pericentric H3K9me3 formation by HP1 interaction-defective histone methyltransferase Suv39h1
- 著者
- Daisuke Muramatsu Hiroshi Kimura Kaoru Kotoshiba Makoto Tachibana Yoichi Shinkai
- 出版者
- 日本細胞生物学会
- 雑誌
- Cell Structure and Function (ISSN:03867196)
- 巻号頁・発行日
- pp.16013, (Released:2016-10-12)
- 被引用文献数
- 1 14
Pericentric regions form epigenetically organized, silent heterochromatin structures that accumulate histone H3 lysine 9 tri-methylation (H3K9me3) and heterochromatin protein 1 (HP1), a methylated H3K9-binding protein. At pericentric regions, Suv39h is the major enzyme that generates H3K9me3. Suv39h also interacts directly with HP1. However, the importance of HP1 interaction for Suv39h-mediated H3K9me3 formation at the pericentromere is not well characterized. To address this question, we introduced HP1 binding-defective, N-terminally truncated mouse Suv39h1 (ΔN) into Suv39h-deficient cells. Pericentric H3K9me3-positive cells were not detected by endogenous-level expression of ΔN. Notably, ΔN could induce pericentric accumulation of H3K9me3 as wild type Suv39h1 did if it was overexpressed. These findings demonstrate that the N-terminal region of Suv39h1, presumably via HP1–Suv39h1 interaction, is required for Suv39h1-mediated pericentric H3K9me3 formation, but can be overridden if Suv39h1 is overproduced, indicating that Suv39h1-mediated heterochromatin formation is controlled by multiple modules, including HP1.