配列特異の転写因子の異位はミトッククロマチンから発生する
M A Martínez-Balbás1, A Dey, S K Rabindran
1Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Cell
|October 6, 1995
まとめ
ミトーシスでは,ストレス誘発性ヒト熱ショックタンパク質70 (hsp70) の遺伝子発現が抑制されます. 転写因子はhsp70プロモーターから異動しており,クロマチンの構造がこのミトス抑制に影響を及ぼすことを示唆しています.
科学分野:
- 分子生物学は分子生物学である.
- 細胞生物学 細胞生物学
- 遺伝学 遺伝学とは
背景:
- 転写活動は,一般的にミトーシス中に抑制されます.
- ストレス誘発性ヒト熱ショックタンパク質70 (hsp70) 遺伝子の発現はミトーシス中に廃止されます.
研究 の 目的:
- ミトーシス中のhsp70遺伝子発現の抑制の背後にあるメカニズムを調査する.
- ミトス抑制における転写因子とクロマチンの構造の役割を特定する.
主な方法:
- ミト細胞抽出物における転写因子 (C/EBP,GBP,HSF1,Sp1) のDNA結合活動の分析.
- 転写因子の局所化を評価するために,in vivo足跡と免疫細胞化学分析を行う.
- 染色体構造を評価するためのDNase I過敏性アッセイ.
主要な成果:
- C/EBP,GBP,HSF1の結合活動は正常であったが,Sp1はミトーシス中にhsp70プロモーターへの結合が低下した.
- すべてのシーケンス固有の転写因子は,ミトーシス過程でプロモーターシーケンスと大量クロマチンから位移した.
- ミトティッククロマチンは,hsp70プロモーターにDNase I過敏性を保持しており, kanonical nucleosome構造に組織されていないことを示しています.
結論:
- クロマチンの凝縮は,転写因子シフトと相関しており,hsp70.0のミトーシス抑制におけるクロマチンの構造の役割を示唆しています.
- ミトスの染色体からの転写因子の移転は,ミトスの後の転写プログラムを再設定するための潜在的なメカニズムを提供します.
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