染色体特異的な転写延長因子FACTは,ヒトのSPT16およびSSRP1タンパク質で構成されています
G Orphanides1, W H Wu, W S Lane
1Howard Hughes Medical Institute, Department of Biochemistry, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway 08854, USA.
Nature
|July 27, 1999
まとめ
クロマチン構造は遺伝子発現を調節する. Spt16/Cdc68とSSrp1を含むFACT複合体は,核細胞と相互作用してクロマチンの転写を促進し,延長中に分解を促進します.
科学分野:
- 分子生物学は分子生物学である.
- 遺伝子規制 遺伝子規制
- クロマチンの生物学
背景:
- 遺伝子発現の調節は,クロマチンの構造に極めて依存しています.
- 裸のDNAトランスクリプションは最小限の要素で効率的ですが,クロマチンのテンプレートによるトランスクリプションにはアクセサリー要因が必要です.
- ATP依存のクロマチンリモデレータとヒストンアセチルトランスフェラーゼは,転写の開始を促進する.
研究 の 目的:
- FACT (ファシリテート・クロマチン・トランスクリプション) 複合体の成分を特定する.
- 染色体転写におけるFACTの役割を明らかにする.
- FACTが転写延長を促進するメカニズムを調査する.
主な方法:
- FACT複合体の生化学的浄化と特徴付け.
- 酵母遺伝学では,Spt16/Cdc68.8のインビボ機能を研究する.
- クロマチンテンプレートを用いたインビトロ転写アッセイ.
- ヌクレオソームとヒストン二次体とのFACT相互作用の分析.
主要な成果:
- FACTは,ヒトのSpt16/Cdc68ホモログとSSrp1.1で構成されています.
- 酵母SPT16/CDC68は不可欠であり,体内でのトランスクリプトの延長に関与しています.
- FACTは核細胞とヒストンのH2A/H2B二次体と相互作用する.
- FACTの活動は,クロスリンクする核細胞ヒストンによって抑制されます.
結論:
- FACTは,クロマチン特異的な主要な延長因子である.
- FACTは,トランスクリプション中に核細胞分解を促進することによって機能する可能性が高い.
- Spt16/Cdc68は,体内でのトランスクリプトの延長に重要な役割を果たしています.
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