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Published on: May 21, 2020
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Ded1pの凝縮は,家事からストレスタンパク質の生産への変換スイッチを促進します
Christiane Iserman1, Christine Desroches Altamirano2, Ceciel Jegers1
1Max Planck Institute of Molecular Cell Biology and Genetics, Pfotenhauerstraße 108, 01307 Dresden, Germany.
Cell
|May 4, 2020
まとめ
細胞は高温に耐えるために 熱ショック反応を利用します タンパク質Ded1pは 変換を制御する凝縮体を形成し 家庭管理遺伝子を抑制し ストレス遺伝子を活かします
科学分野:
- 細胞生物学
- 熱ショック反応の分子機構
- タンパク質相分離
背景:
- 細胞は高温に熱ショック反応を起こし 遺伝子発現が変化します
- 具体的メカニズムは,特に翻訳レベルでは,完全に理解されていません.
研究 の 目的:
- 熱ショック反応における変換開始因子の役割を調査する.
- 細胞が熱ストレスで遺伝子発現をどのように調節するかを解明する.
主な方法:
- 芽生えた酵母をモデル生物として利用した.
- リボソームプロファイリングとインビトロトランスレーションアッセイを用いた.
- Ded1pの変種と様々な種の同種を分析した.
主要な成果:
- 本質的な変換開始因子Ded1pは,熱誘導によるフェーズ分離をゲル状のコンデンサートにします.
- コンデンサートの形成はDed1pを無効化し,ストレスのmRNAの翻訳を促進しながら,家事mRNAの翻訳を抑制します.
- Ded1p凝縮は適応性があり,生物の最大成長温度に最適化されています.
結論:
- Ded1p凝縮は熱ショック反応の重要な構成要素です.
- このメカニズムは,厳しい熱ストレス下での生存を高めるために,選択的に mRNA 翻訳を抑制します.
- タンパク質の相分離は,細胞のストレス適応における新しい調節層を提供します.
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