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ミトコンドリアストレスは,長寿とUPRを促進するクロマチンの再編成を誘導する
Ye Tian1, Gilberto Garcia1, Qian Bian2
1Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA 94720, USA; The Glenn Center for Aging Research, University of California, Berkeley, Berkeley, CA 94720, USA.
Cell
|May 3, 2016
まとめ
生物はミトコンドリアのストレスを管理するために表遺伝子の改変を利用し,遺伝子を選択的に発現させるためにクロマチンの構造を変更する. この反応は 代謝の健康を促進し 生命の初期に 保護メカニズムを確立することで 寿命を延ばします
科学分野:
- 細胞生物学
- エピジェネティクス
- ミトコンドリア機能
背景:
- 生物はミトコンドリアのストレスと代謝機能障害に反応して 保護遺伝子を活性化します
- この反応は生物の生涯にわたって持続し,長期的な健康に影響を与えます.
- エピジェネティックメカニズムは ストレス反応中の遺伝子発現を 調節するのに不可欠です
研究 の 目的:
- ミトコンドリアのストレス反応におけるクロマチンの構造と表遺伝子学的変化の役割を調査する.
- これらのエピジェネティックの変化を媒介する重要な分子プレーヤーを特定する.
- これらの改変が選択的遺伝子発現と寿命を延ばすのにどのように貢献するのかを理解する.
主な方法:
- ミトコンドリアのストレスに対するクロマチン構造の変化の分析.
- ヒストンH3K9の二甲基化パターンの調査
- ヒストンメチルトランスフェラーゼメット-2と核共因子lin-65を重要な成分として特定する.
- DVE-1のようなストレス反応因子の オープンクロマチン領域への結合を評価する
主要な成果:
- ミトコンドリアのストレスは,ヒストンH3K9の二甲基化によって特徴づけられるクロマチンの構造の広範な変化を誘発する.
- ヒストンメチルトランスフェラーゼmet-2と核共因子lin-65は,ストレス反応中のH3K9二メチル化に不可欠である.
- グローバルクロマチンは静止されても 特定の領域は開き DVE-1のような因子の結合を可能にします
- これらのエピジェネティックな改変は,選択的な遺伝子発現を容易にする.
結論:
- ミトコンドリアのストレスは,遺伝子発現を調節するためにヒストンH3K9の二メチル化を含む特定の表遺伝子変異を誘発する.
- met-2とlin-65複合体は,これらの静音マークを確立する上で重要な役割を果たします.
- 選択的なクロマチンの開きによって ストレス反応性の遺伝子が活性化され 寿命が延びるのです
- エピジェネティック再プログラミングは 成人期に代謝ストレス反応を 広めるための基本的メカニズムです
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