イーストキネトコアを,ユビキチン依存性分解とSkp1p媒介のリン酸化によって調節する
K B Kaplan1, A A Hyman, P K Sorger
1Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA.
Cell
|December 9, 1997
まとめ
Cbf3複合体は,酵母におけるキネトコア組成に不可欠である. 研究者らは,p23Skp1が,リン酸化経由でp58Ctf13を活性化させ,複合体の組み立てをセントロメア複製に結びつけることを発見した.
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.
- 遺伝学 遺伝学とは
背景:
- S. cerevisiaeのCbf3複合体は,センターメリックDNA (CDEIII) と結合し,キネトコア組立を開始する.
- キネトコア組立は,細胞分裂中の適切な染色体分離に不可欠です.
研究 の 目的:
- 再結合タンパク質からCbf3複合体を再構成する.
- Cbf3複合体内のp58Ctf13およびp23Skp1サブユニットの役割を分析する.
- Cbf3複合体の機能を制御する規制メカニズムとその中心粒子の複製との関係を解明する.
主な方法:
- 再結合タンパク質発現と複合分解.
- タンパク質とタンパク質の相互作用の生化学分析.
- リン酸化測定は,キナーゼ活性を決定する.
- ウビキチン化とプロテアソームの分解に関する研究.
主要な成果:
- p23Skp1は,リン酸化によってp58Ctf13を活性化する.
- p58Ctf13は,プロテアソームの分解を標的とした不安定なタンパク質です.
- Scul ((Cdc4) は,おそらくp58Ctf13のユビキチネーションを媒介する.
- p23Skp1は,酵母体においてG1およびG2特異な機能の両方を表しています.
結論:
- Cbf3複合体の構成は,p58Ctf13のリン酸化 (活性化) とユビキチン化 (分解) のバランスによって制御される.
- この結合されたアクティベーションと破壊メカニズムは,Cbf3複合体の組み立てをS相中のセントロメア複製と結びつける.
- これらの規制のステップを理解することは,細胞サイクル制御とゲノム安定性を理解する鍵です.
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