RNAポリメラーゼIIの停止は,精密な遺伝子調節を可能にするために,DNA指定の核細胞組織を混乱させます
Daniel A Gilchrist1, Gilberto Dos Santos, David C Fargo
1Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.
Cell
|November 16, 2010
まとめ
調節されたRNAポリメラーゼII (Pol II) の一時停止は,高度に調節された遺伝子における抑圧的なクロマチンの形成を防ぐ. このメカニズムは,プロモーターの占有について核細胞と競争し,遺伝子の活性化を促進します.
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:
- メタゾアンの転写は,プロモーターの募集またはRNAポリメラーゼII (Pol II) の一時停止に依存しています.
- 異なる規制戦略は,デフォルトのクロマチン構造の違いと相関する.
研究 の 目的:
- 遺伝子調節におけるDNA配列,クロマチンの構造,およびPol IIの一時停止との関係を調査する.
- プロモーターアクセシビリティと遺伝子活性化における,一時停止したPol IIの役割を理解する.
主な方法:
- 高度調節遺伝子のクロマチンの構造とPol IIの占有率の比較分析と,管理遺伝子の比較分析.
- 核細胞形成の傾向を予測するためにDNA配列のインシリコ分析.
主要な成果:
- 高度に調節された遺伝子はPol IIの休止を示し,DNA配列は遺伝子内の核細胞形成を不利にしますが,プロモーター閉塞を好みます.
- 顕著なPol IIの休止が欠けている管理遺伝子は,より高い下流の核染色体占有率と核染色体欠乏プロモーターを示しています.
- Paused Pol IIは,高度に調節された遺伝子のプロモーターの占有について,核分裂体と積極的に競合する.
結論:
- Paused Pol IIは,高度に調節された遺伝子のプロモーターにおける抑圧的な染色体形成を防止する上で重要な役割を果たします.
- この競争メカニズムは,プロモーターのアクセシビリティを確保し,遺伝子活性化と将来の転写イベントを促進します.
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