CDK-APC/Cオシレータは,主に周期的な細胞サイクルトランスクリプションを誘導する
Sahand Jamal Rahi1, Kresti Pecani2, Andrej Ondracka2
1Laboratory of Cell Cycle Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA; Center for Studies in Physics and Biology, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
Cell
|April 9, 2016
まとめ
細胞サイクル遺伝子発現は主にCDK-APC/Cタンパク質によって制御される. しかし,SIC1遺伝子は,ミトスサイクリンが低い場合でも核分裂を促進し,故障防止として機能します.
科学分野:
- 細胞生物学
- 分子生物学
- 遺伝学
背景:
- 細胞循環の進行には 振動する遺伝子発現が伴うので 調節に不可欠です
- 重要な質問は,この振動がCDK-APC/Cタンパク質によって中央的に制御されるのか,それとも分散型転写因子 (TF) カスケードによって制御されるのかである.
研究 の 目的:
- 芽生える酵母における細胞サイクル進行中の遺伝子発現の規制メカニズムを調査する.
- CDK-APC/Cタンパク質とTFカスケードがトランスクリプトの振動を制御する役割を決定する.
主な方法:
- ゲノム全体の転写を評価するためにRNA-sequencing (RNA-seq)
- 単細胞光顕微鏡で遺伝子発現の動態を観察する.
- 数学的モデルと実験的検証
主要な成果:
- CDK-APC/Cタンパク質は,芽生えた酵母におけるほぼすべての遺伝子の転写を指示する.
- 3つの例外的な遺伝子は,CDK-APC/Cの逮捕時にパルサティルな転写パターンを表します.
- B型サイクリンを阻害するSIC1のトランスクリプトは詳細に研究された.
結論:
- この研究は,Sic1が故障防止メカニズムとして機能する証拠を提供します.
- シク1は核分裂を促し,ミトスサイクリンレベルが低くなると,直感に反する発見です.
- これは主に集中的なシステム内の特定の遺伝子の分散型規制の役割を強調しています.
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