Mpk1 MAPKとPaf1複合体の関連は,Sen1媒介の早期転写終止をブロックする
1Department of Molecular and Cell Biology, Boston University Goldman School of Dental Medicine, Boston University, Boston, MA 02118, USA.
Cell
|March 8, 2011
まとめ
Mpk1経路は,Paf1複合体と相互作用することによって,酵母における遺伝子転写の延長を調節し,早期の遺伝子終了を防ぐ. ミトゲン活性化タンパク質キナーゼ (MAPK) と転写延長因子を含むこのメカニズムは,ヒト細胞に保存されています.
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
- イースト細胞生物学 イースト細胞生物学
背景:
- Mpk1 MAPK経路は,酵母細胞壁の整合性にとって極めて重要です.
- Mpk1は,プロモーター領域における非触媒的メカニズムを通じて,ストレス誘発遺伝子の転写を活性化します.
研究 の 目的:
- 転写延長におけるMpk1の役割を調査する.
- ストレス反応中にMpk1が遺伝子発現に影響を与える非触媒的メカニズムを解明する.
主な方法:
- イーストにおけるMpk1とPaf1の相互作用の遺伝子分析.
- 遺伝子特異的検査を用いた転写延長欠陥の調査.
- 終結因子Sen1,Nrd1,Nab3の役割を研究する3.
- 人間のERK5 MAPKと人間のPaf1.1との比較分析
主要な成果:
- Mpk1は,Paf1C複合体のPaf1サブユニットと相互作用し,その触媒活動とは独立しています.
- この相互作用を妨害するPaf1変異は,Mpk1誘発遺伝子の誤った転写延長につながります.
- この欠陥は,Sen1とNab3によって媒介された早めの転写終止によるものです.
- Mpk1は,Sen1-Nrd1-Nab3終結複合体を抑制することによって,転写の衰弱を防ぐ.
結論:
- Mpk1は,転写の開始と延長において二重の役割を果たしています.
- Mpk1の延長における機能は,Paf1Cとの相互作用によって早産を防ぐことを含む.
- この調節メカニズムは進化的に保存されており,ヒトのERK5とPaf1は類似の相互作用を示しています.
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