エピジェネティクス. H3K9メチル化による限られた表遺伝子遺伝
Pauline N C B Audergon1, Sandra Catania1, Alexander Kagansky1
1Wellcome Trust Centre for Cell Biology and Institute of Cell Biology, School of Biological Sciences, The University of Edinburgh, Max Born Crescent, Edinburgh EH9 3BF, Scotland, UK.
Science (New York, N.Y.)
|April 4, 2015
まとめ
ヒストンH3ライシン9 (H3K9) メチル化は遺伝性表遺伝子マークである. その遺伝は通常,活性除去によって防止されますが,Epe1デメチラーゼをブロックすると,安定した伝播が可能になります.
科学分野:
- エピジェネティクス エピジェネティクス
- 分子生物学は分子生物学である.
- クロマチンの生物学
背景:
- トランスレーション後のヒストンの改変は,表遺伝子遺伝において極めて重要です.
- ヒストンH3ライシン9 (H3K9) メチル化がヘテロクロマチン形成に不可欠である.
- 以前は,H3K9メチル化の表遺伝的遺伝性に関する証拠は存在しなかった.
研究 の 目的:
- H3K9メチル化の表遺伝的遺伝性を示すために.
- H3K9メチル化遺伝を調節するメカニズムを調査する.
- H3K9メチレーション伝播を阻害する要因を特定する.
主な方法:
- 単一のH3K9メチルトランスフェラーゼ,Clr4.4を持つ利用された分裂酵母.
- H3K9メチル化を制御するために,解放可能な縛られたClr4を使用しています.
- メチル化維持を観察するためにヒストン脱メチラーゼEpe1を非活性化しました.
主要な成果:
- H3K9メチル化の活性消去は,野生型細胞では急速に発生する.
- Epe1の無活性化により,複数の細胞分裂を通してH3K9のメチル化維持が可能になった.
- H3K9メチル化は,Epe1不活性化後のメオシス経由で世代を超えて遺伝された.
結論:
- ヒストンH3ライシン9 (H3K9) メチル化は,表遺伝的に遺伝するマークです.
- Epe1による活性脱メチル化は,通常,ヘテロクロマチンの無許可の遺伝を防ぐ.
- これらのメカニズムを理解することは,表遺伝的状態を制御する鍵です.
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