オートファギーの停止とmTORによって調節されるリソソームのリフォーム
Li Yu1, Christina K McPhee, Lixin Zheng
1Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
Nature
|June 8, 2010
まとめ
オートファギーは,飢餓中に細胞の成分をリサイクルします. この研究では,mTOR再活性化による栄養素感知がライソソームを再生し,細胞機能を維持するサイクルが明らかになりました.
科学分野:
- 細胞生物学 細胞生物学
- 分子生物学は分子生物学である.
- 生理学 生理学とは
背景:
- オートファギーは,細胞プラズマ成分を分解するための保存された細胞プロセスです.
- ラパミシン (TOR) シグナル伝達の栄養素反応性キナーゼ標的は,栄養素の豊富さ中にオートファギーを阻害する.
- 飢餓中のオートファジーとリソソーム運命を調節する方法は,完全に理解されていません.
研究 の 目的:
- 長期的飢餓中のオートファジーとmTORシグナル伝達の調節を調査する.
- 栄養素感知とオートファギーにおけるリソソームホメオスタシスの役割を明らかにする.
主な方法:
- ネズミの腎臓細胞を用いて,オートファジーとmTORシグナル伝達を研究した.
- オートファギー依存のmTOR再活性化が研究されている.
- 飢餓中のライソソーム生物発生とホメオスタシスを調べました.
主要な成果:
- mTORシグナル伝達は,最初はオートファギーの開始時に抑制され,長期間の飢餓中に再活性化されます.
- mTORの活性化は,オートリソソーム産物の分解に依存している.
- このプロセスは新しいリゾソームを生成し,種間の細胞におけるリゾソーム補完体を回復させます.
結論:
- 保存されたオートファギーのサイクルが,飢餓中のリソソームホメオスタシスに栄養分感を結びつける.
- mTORシグナル伝達の再活性化は,オートファギーを弱め,ライソソームの再生を促進する.
- このメカニズムは,栄養素欠乏時に細胞の栄養供給とリソソーム機能を確保します.
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