飢餓が誘発した酵母の微分化には,キャップ・インディペンデント・トランスレーションが必要です
Wendy V Gilbert1, Kaihong Zhou, Tamira K Butler
1Department of Molecular and Cell Biology, Department of Chemistry, and Howard Hughes Medical Institute, University of California, Berkeley, CA 94720, USA.
Science (New York, N.Y.)
|September 1, 2007
まとめ
細胞内リボソームのエントリーサイト (IRES) は,ストレス中にタンパク質合成を可能にします. この研究は,酵母菌の侵入性成長におけるIRES機能の新しいメカニズムを明らかにし,その生理学的重要性を実証しています.
科学分野:
- 分子生物学は分子生物学である.
- イースト遺伝学 イースト遺伝学
- 遺伝子規制 遺伝子規制
背景:
- 細胞内リボソームエントリーサイト (IRES) は,環境ストレス中にキャップ独立翻訳を開始することが提案されている翻訳されていないmRNA領域です.
- 細胞IRESの生理学的役割と分子機構は,大部分が特徴づけられていないままである.
研究 の 目的:
- 酵母における細胞IRESの機能とメカニズムを調査する.
- イーストの侵入性成長におけるIRES媒介トランスレーションの役割を決定する.
主な方法:
- 侵襲的な成長に関与する7つの酵母遺伝子の分析.
- これらの遺伝子内のIRES要素の識別と特徴付け.
- 翻訳開始因子 (eIF4G) の必要性を調査する.
- 5'UTR A豊富な元素とポリ (Pab1) 結合タンパク質 (Pab1) の募集の役割を評価する.
- 5'UTRの変異分析により,IRESの活動と侵襲的な増殖を評価する.
主要な成果:
- 侵襲的な成長に不可欠な7つの酵母遺伝子は,強力なIRESを持っています.
- これらのIRESは,上限独立翻訳の開始因数eIF4Gに依存しています.
- 5'UTRの構造化されていない,Aに富んだ要素がPab1を勧誘し,内部イニシアチブを媒介する.
- このメカニズムは,RNA構造に依存するウイルスIRESと異なる.
- 5'UTR変異がIRESの活動を妨害すると,侵襲的な成長が損なわれます.
結論:
- 細胞IRESは,酵母菌の侵入的成長において,生理学的機能が実証されている.
- IRESによるキャップ・インデペンデント・トランスレーションは,ストレスへの適応において極めて重要です.
- 特定されたメカニズムは,ウイルスのIRESメカニズムとは異なるA豊富な要素を通じてPab1の採用を伴う.
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