APC ((Cdc20) は,アナフェーズ阻害体 Pds1 とサイクリン Clb5 を破壊することによって,ミトーシスからの脱出を促進します
M Shirayama1, A Tóth, M Gálová
1Research Institute of Molecular Pathology, Vienna, Austria.
Nature
|January 26, 2000
まとめ
アナフェーズ促進複合体/サイクロソーム (APC/C) は細胞分裂を制御する. 酵母体では,APC/Cは,Cdc14の放出のためにPds1の分解を標的とし,これはミトスの脱出と細胞増殖に不可欠である.
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.
- バイオケミストリー バイオケミストリー
背景:
- アナフェーズ促進複合体/サイクロソーム (APC/C) によるウビキチン媒介タンパク質分解は,細胞サイクル進行において極めて重要です.
- Cdc20やCdh1/Hct1のようなサブユニットによって調節されるAPC/C活動は,姉妹染色体の分離とミトスの脱出を促します.
- Cdc14フォスファタゼは,Cdh1の活性化とSic1の蓄積を含むミトの脱出に不可欠ですが,その放出メカニズムは不明です.
研究 の 目的:
- Cdc14フォスファタゼの活性化におけるCdc20 (APC(Cdc20)) に結合するAPC/Cの役割を明らかにする.
- APC (((Cdc20) 媒介によるタンパク質分解が,Saccharomyces cerevisiaeにおけるミトスの脱出と細胞増殖にどのように寄与するかを調査する.
- Cdc14の活性化およびその後の細胞サイクルイベントに不可欠な APC ((Cdc20) の特定の基板を決定する.
主な方法:
- 酵母遺伝子をSaccharomyces cerevisiaeで利用しました.
- アナフェーズ促進複合体/サイクロソーム (APC/C) によって媒介されるタンパク質分解経路を調査した.
- ミトーシスにおけるPds1,Clb5,Cdc14,Cdc20,Cdh1,Sic1の役割を分析した.
主要な成果:
- APC(Cdc20) は,Pds1とS相サイクリンClb5.5の分解を媒介する.
- 核からCdc14フォスファタゼの放出には,Pds1の分解が必要である.
- Clb5の分解は,Cdc14がCdk1を無効化し,Cdh1とSic1を活性化するために不可欠であり,ミトスの脱出を促進します.
- Pds1とClb5の両方が欠けている細胞は,Cdc20なしで増殖することができます.
結論:
- APC ((Cdc20) は,Pds1とClb5.5を分解することによって,ミトスの脱出を促進する二重の役割を果たします.
- APC ((Cdc20) によるPds1の分解はCdc14の放出の前提条件であり,Clb5の分解はCdc14のダウンストリーム機能に不可欠である.
- この発見は,ミトスの脱出のための重要な規制メカニズムを明らかにし,特定の突然変異の背景におけるAPC/C機能の冗長性を強調しています.
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