mRNAデカッピングのアクティベーターによる一般的な翻訳抑制
1Howard Hughes Medical Institute, Department of Molecular and Cellular Biology, University of Arizona, Tucson, Arizona 85721, USA.
Cell
|September 24, 2005
まとめ
Dhh1pとPat1pタンパク質は,翻訳を抑制し,処理器官におけるmRNAの分解を促進する. 彼らの活動は翻訳のバランスを保ち,細胞の制御に影響を与えます.
科学分野:
- 分子生物学は分子生物学である.
- 細胞生物学 細胞生物学
- 遺伝学 遺伝学とは
背景:
- ユカリオットmRNAの運命は,翻訳終了とメッセンジャーリボ核タンパク質 (mRNP) 複合体への組み立てを含む.
- これらのmRNPは処理体 (P体) に蓄積され,これはmRNAの分解と分解機構の主要な場所である.
- トランスレーションからmRNAの分解への移行を理解することは,細胞の調節に極めて重要です.
研究 の 目的:
- mRNAの翻訳からP体蓄積への移行に関与するタンパク質を特定する.
- 翻訳制御とP体形成におけるデカッピング活性化剤 Dhh1pとPat1pの役割を解明する.
- Dhh1pとPat1pがmRNAの運命を調節するメカニズムを調査する.
主な方法:
- Dhh1pとPat1pが欠けているか,過剰に発現している酵母菌株の遺伝子分析.
- Dhh1p.p.を使用したインビトロ翻訳アッセイ.
- トランスレーション開始の阻害を含むインビボ実験.
主要な成果:
- Dhh1pとPat1pは,トランスレーション抑制剤とP体形成の促進剤として機能する.
- Dhh1pとPat1pが欠乏している株は,mRNAデカッピング,P体形成,およびトランスレーション抑制の欠陥を示します.
- Dhh1pまたはPat1pの過剰発現は,翻訳抑制,P体形成,および成長停止につながる.
- Dhh1pとそのヒト同型RCK/p54は,インビトロで翻訳を抑制し,この抑制は,インビヴォで翻訳開始を阻害することによって回避されます.
結論:
- Dhh1pとPat1pは,切断のためのmRNAをターゲットとする翻訳抑制の保存されたメカニズムを媒介する.
- このメカニズムは翻訳管理の不可欠な部分であり,アクティブ翻訳と競争的にバランスをとります.
- このバランスを変化させることは,トランスレーションレベルでの遺伝子発現の調節の根本的な側面です.
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