Cdc6は,Sic1およびHct1と協力して,ミトーシックサイクリン依存キナーゼを無効化する

A Calzada¹, M Sacristán, E Sánchez

¹Instituto de Microbiología-Bioquímica, Departemento de Microbiología y Genética, Universidad de Salamanca, CSIC, Spain.

Nature

|July 19, 2001

まとめ

芽生えた酵母では,DNA複製因子であるCdc6も,サイクリン依存キナーゼ (CDKs) を阻害してミトスの退去を促進します. この二重の役割は,適切な細胞サイクル進行とDNA複製の開始を保証します.

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.
イースト遺伝学イースト遺伝学

背景:

Saccharomyces cerevisiaeにおけるミトスの脱出には,サイクリン依存キナーゼ (CDK) の不活性化が必要です.
この無活性化は,B-サイクリンの分解とSic1.1による阻害によって達成される.
DNA複製因子であるCdc6は,CDK結合と転写制御を含むSic1と類似性を共有しています.

研究の目的:

CDKの無活性化とミトスの退出におけるCdc6の役割を調査する.
Cdc6が,DNA複製における既知の役割を超えて,CDK活動の調節に寄与するかどうかを決定する.

主な方法:

Cdc6ドメインに欠損したSaccharomyces cerevisiae株の遺伝子分析.
ミトスの脱出タイミングとCDKの活性度の評価.
複製前複合体の形成の評価.

主要な成果:

Cdc6は,後期ミトーシス中のCDK無活性化に寄与する.
Cdc6のCDKと相互作用するドメインの削除は,特にSic1が欠けている場合やサイクリン分解が妨げられている場合,ミトスの脱出を遅らせます.
CDK不活性化におけるCdc6の役割は,後のDNA複製のための条件を確立するために重要である.

結論:

Cdc6は二重の機能を持ち,ミトスの脱出とDNA複製の両方を調節します.
CDKsのCdc6不活性化は,細胞サイクルを通ってタイムリーに進行するために不可欠です.
この研究は,ミトスの脱出とDNA複製の開始を結びつける新しい規制メカニズムを明らかにしています.

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