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5' UTR m(6)A キャップ・インデペンデント・トランスレーションを推進する
Kate D Meyer1, Deepak P Patil1, Jun Zhou2
1Department of Pharmacology, Weill Medical College, Cornell University, New York, NY 10065, USA.
Cell
|November 24, 2015
まとめ
メッセンジャーRNA (mRNA) 翻訳は5'キャップとは独立して起こる. 5'非翻訳領域 (UTR) のN(6) -メチラデノシン (m(6) は,特に細胞ストレス中に直接翻訳機構を勧誘する.
科学分野:
- 分子生物学
- RNA 生物学
- 遺伝子発現の規制
背景:
- タンパク質翻訳は通常,キャップ結合複合体による5'キャップ認識によって開始される.
- キャップ・インデペンデント・トランスレーション・メカニズムは十分に理解されていない.
- N(6) -メチラデノシン (m(6) Aは一般的なmRNA変異である.
研究 の 目的:
- 5' UTR m(6) Aのキャップ独立変換における役割を調査する.
- 5' UTR m(6) Aが変換を促進するメカニズムを解明する.
- このメカニズムの重要性を 細胞のストレスで判断する.
主な方法:
- 5' UTR に m(6) A を導入または削除するためのサイト指向型変異.
- ユカリオット開始因子3 (eIF3) とm(6) Aの結合を評価する生化学的測定
- インビトロ翻訳試験
- 熱ショック後のHsp70 mRNA翻訳の分析
- トランスクリプトーム全体のm ((6) 様々なストレス条件下でのプロファイリング.
主要な成果:
- 5' UTR の単一の m(6) A は,キャップ独立変換を媒介するのに十分である.
- 5' UTR m(6) AはeIF3に直接結合し,43Sのリボソーム複合体の募集を容易にする.
- アデノシンメチレーションの阻害は,特に5' UTR m(6) Aを含むmRNAの翻訳を阻害する.
- 熱ショックにより,Hsp70 mRNAのm(6) Aレベルが上昇し,そのキャップ独立翻訳を促進する.
- 細胞のストレスはm(6) Aの全体的な再配分を引き起こし,5' UTR m(6) Aの修正を増加させます.
結論:
- 5' UTR m(6) Aは,eIF3を直接利用することで,上限独立の翻訳を開始できます.
- この経路は,細胞のストレス条件下で選択的なmRNA翻訳のためのメカニズムを提供します.
- ストレス反応中の遺伝子発現を制御するスイッチとして作用する.
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