NUFIP1は,飢餓によるリボファギーのリボソーム受容体である
Gregory A Wyant1,2,3,4, Monther Abu-Remaileh1,2,3,4, Evgeni M Frenkel1,2,3,4
1Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Science (New York, N.Y.)
|April 28, 2018
まとめ
核脆弱X精神遅延相互作用タンパク質1 (NUFIP1) は選択性リボソーム自 (リボファジー) の受容体として作用する. このプロセスは,飢餓中の細胞生存に不可欠であり,NUFIP1がLC3Bに結合し,リボソームをオートファゴソームに提供することを含む.
科学分野:
- 細胞生物学
- 分子生物学
- オートファギーの研究
背景:
- リソソームは,マクロ分子分解,栄養素感知,およびmTORC1 (ラパミシン複合体1のメカニズム標的) に関する重要な臓器である.
- リソソーム機能は様々な人間の病気に絡み合っており,その動的調節を理解する必要性を強調しています.
- mTORC1のシグナル伝達は細胞の成長と代謝の重要なレギュラーであり,栄養素の利用可能性に影響する.
研究 の 目的:
- 栄養分レベルとmTORシグナリングがライソソームプロテオームを動的に調節する方法を調査する.
- mTORC1抑制に反応するリンパ体機能に関わるタンパク質を特定する.
- 細胞のストレス反応とオートファギーにおけるNUFIP1の役割を明らかにする.
主な方法:
- 素早く分離されたリソソームの定量タンパク質分析
- mTORC1の抑制によるタンパク質再分布の調査は,免疫降水および顕微鏡などの技術を用いて行われます.
- タンパク質とタンパク質の相互作用,特にNUFIP1,LC3Bとリボソームの相互作用を決定する生化学的測定法.
主要な成果:
- 栄養分レベルとmTORシグナリングは,リソソームタンパク質を動的に調節することが判明しました.
- mTORC1を阻害すると,NUFIP1 (核脆性X精神遅延相互作用タンパク質1) は核からオートファゴソームとリソソームに転移する.
- NUFIP1はLC3B (微小管関連タンパク質1A/ 1B 軽鎖3B) に直接結合し,リボソームを自己ファゴソームに分解させるのを促進する.
結論:
- NUFIP1は,リボソームの選択的オートファギー,すなわちリボファギーと呼ばれるプロセスにおいて重要な役割を果たします.
- NUFIP1によるリボファギーは,飢餓状態での細胞生存に不可欠です.
- NUFIP1は受容体として機能し,リボソームをLC3B経由でオートファージ機構と結びつける.
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