Cln3は,SBF結合レプレッサーWhi5のリン酸化を経由してG1特異的転写を活性化します
Robertus A M de Bruin1, W Hayes McDonald, Tatyana I Kalashnikova
1Department of Molecular Biology, 10550 North Torrey Pines Road, La Jolla, California 92037, USA.
Cell
|June 24, 2004
まとめ
Whi5は芽生えた酵母におけるG1特異の転写抑制剤として作用し,細胞サイクル開始を制御する. その無活性化により,Cln3/CDKの要件を回避し,細胞循環調節におけるその役割を明らかにする.
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.
- 遺伝学 遺伝学とは
背景:
- 芽生えた酵母細胞サイクルは,Cln3/cyclin依存キナーゼ (CDK) によって駆動されるG1特異の転写活性化によって開始されます.
- Cln3/CDKの直接標的を特定することは,細胞サイクル制御メカニズムを理解するために不可欠です.
研究 の 目的:
- 細胞サイクル開始に関与するCln3/CDKの新しい標的を特定する.
- G1固有の遺伝子調節と細胞サイクル進行の文脈でWhi5の機能を明らかにする.
主な方法:
- 多次元タンパク質相互作用技術 (MudPIT) は,SBFとMBFの転写因子複合体を分析するために使用されました.
- Whi5の不活性化と過剰発現を含む機能的測定が行われました.
- G1特異のプロモーターとWhi5関連性の分析と,Whi5解離に対するCln3/CDKの影響.
主要な成果:
- Whi5はSBF転写因子複合体の構成要素として特定されましたが,MBFではありません.
- Whi5不活性化により,G1遺伝子発現と芽生えが早まり,Cln3.3の必要性が回避されました.
- Whi5は, Cln3/CDKのリン酸化によって促進されるプロセスである転写活性化時にG1プロモーターから離散する.
結論:
- Whi5は,哺乳類のRb.に類似したG1固有の転写抑制剤として機能する.
- Cln3/CDKは,リン酸化によってWhi5の活性に敵対し,その解離を促進し,細胞サイクル開始を可能にします.
- Whi5は,芽生えた酵母菌のG1からS段階への移行の重要な調節剤です.
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