TATA結合タンパク質が欠けているネズミの細胞におけるRNAポリメラーゼII転写
Igor Martianov1, Stephane Viville, Irwin Davidson
1Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS/INSERM/ULP, B.P. 163, 67404 Illkirch Cédex, Communauté Urbaine de Strasbourg, France.
まとめ
TATA結合タンパク質 (TBP) 遺伝子を非活性化すると,胚の停止が起こりますが,RNAポリメラーゼII (pol II) の転写は持続し,遺伝子発現のためのTBP独立したメカニズムを明らかにします.
科学分野:
- 分子生物学は分子生物学である.
- 遺伝学 遺伝学とは
- 遺伝子規制 遺伝子規制
背景:
- TATA結合タンパク質 (TBP) は,RNAポリメラーゼによる転写始動に不可欠である.
- TBPは,RNAポリメラーゼI,II,IIIの活性に不可欠な一般的な転写因子である.
研究 の 目的:
- 胚の発達と遺伝子転写におけるTBPの役割を調査する.
- 異なるRNAポリメラーゼのTBPへの依存性を in vivoで決定する.
- TBPから独立するトランスクリプションメカニズムの可能性を調査する.
主な方法:
- ホモログの再結合は,ネズミのTBP遺伝子を不活性化するために使用されました.
- 転写活性を測定するために,in situ run-onアッセイを実施した.
- RNAポリメラーゼIIのリン酸化状態を分析した.
主要な成果:
- TBP遺伝子の不活性化により,胚芽細胞の成長停止とアポトーシスが発生した.
- TBPの損失にもかかわらず,RNAポリメラーゼII (pol II) は転写的に活性化し続けました.
- Pol Iとpol IIIの転写が停止し,TBP依存性の差異を示した.
- 野生型の細胞に匹敵する高レベルのpol II転写が観察されました.
結論:
- RNAポリメラーゼは,TBPに差異的な依存性を示す.
- 証拠は,pol II転写の開始と維持のためのTBPから独立したメカニズムを vivo で示唆しています.
- TBPは生命力にとって不可欠ですが,初期の発達におけるポリII転写に限ったものではありません.
関連する概念動画
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