Study of H3K9me reader of mammalian sex-determining gene Sry
| Project/Area Number |
18H02419
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Review Section |
Basic Section 43050:Genome biology-related
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| Research Institution | Osaka University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥17,290,000 (Direct Cost: ¥13,300,000、Indirect Cost: ¥3,990,000)
Fiscal Year 2020: ¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
Fiscal Year 2019: ¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
Fiscal Year 2018: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
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| Keywords | 性分化 / Sryエピゲノム / エピゲノム / クロモドメイン / 性決定 / H3K9メチル化 / クロモドメインタンパク質 / エピゲノム制御 |
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| Outline of Final Research Achievements |
Epigenetic regulation by histone modification is achieved by the cooperative action of writer, eraser and reader of histones. Cdyl family molecules and HP1 family molecules are chromodomain-containing proteins that can recognize methylated H3K9. In this study, we analyzed the functions of Cdyl family molecules and HP1 family molecules in mouse sex differentiation, to clarify their role as the reader molecule of methylated H3K9 at the Sry locus. We established Cdyl, Cdyl2, and HP1α-deficient mice and then observbed their phenotypes. We did not find abnormalities n sexual differentiation in these mice. However, on the contrary to the initial expectation, genetic analysis under the Jmjd1a-deficient background revealed that Cdyl and Cdyl2 positively regulate male development.
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| Academic Significance and Societal Importance of the Research Achievements |
ほ乳類の性決定遺伝子の発現にエピゲノムが重要であることを私たちは過去に報告しました。この成果を踏まえ本研究では、マウスの性決定遺伝子の発現を抑制すると想定される（すなわちメス化を促すと想定される）エピゲノム読み取り分子、Cdylの機能を解析しました。その結果、予想に反して本分子はオス化を促す機能があることが分かりました。今後はCdylと人の性分化疾患の発症とのが関わりが注目されます。
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Report
(4 results)
Research Products
(38 results)
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[Journal Article] Inhibition of histone methyltransferase G9a attenuates liver cancer initiation by sensitizing DNA-damaged hepatocytes to p53-induced apoptosis2021
Author(s)
Takuma Nakatsuka, Keisuke Tateishi*, Hiroyuki Kato, Hiroaki Fujiwara, Keisuke Yamamoto, Yotaro Kudo, Hayato Nakagawa, Yasuo Tanaka, Hideaki Ijichi, Tsuneo Ikenoue, Takeaki Ishizawa, Kiyoshi Hasegawa, Makoto Tachibana, Yoichi Shinkai, Kazuhiko Koike
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Journal Title
Cell Death & Disease
Volume: 12
Pages: 99-111
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] Deletion of Histone Methyltransferase G9a Suppresses Mutant Kras-driven Pancreatic Carcinogenesis Carcinogenesis2020
Author(s)
Hiroyuki Kato, Keisuke Tateishi*, Hiroaki Fujiwara, Hideaki Ijichi, Keisuke Yamamoto, Takuma Nakatsuka, Miwako Kakiuchi, Makoto Sano, Yotaro Kudo, Yoku Hayakawa, Hayato Nakagawa, Yasuo Tanaka, Motoyuki Otsuka, Yoshihiro Hirata, Makoto Tachibana, Yoichi Shinkai, Kazuhiko Koike
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Journal Title
Cancer Genomics - Proteomics
Volume: 17
Pages: 695705-695705
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] Combined loss of JMJD1A and JMJD1B reveals critical roles for H3K9 demethylation in the maintenance of embryonic stem cells and early embryogenesis.2018
Author(s)
Kuroki, S., Nakai, Y., Maeda, R., Okashita, N., Akiyoshi, M., Yamaguchi, Y., Kitano, S., Miyachi, H., Nakato, R., Ichiyanagi, K., Shirahige, K., Kimura, H., Shinkai, Y., and Tachibana, M.
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Journal Title
Stem Cell Reports
Volume: 10
Pages: 1340-1354
DOI
NAID
Related Report
Peer Reviewed / Open Access
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