TORシグナル伝達経路は,栄養素によって調節される転写因子の核の局所化を制御する
Nature
|December 22, 1999
まとめ
イーストのTORシグナル伝達経路は,重要な転写因子を細胞プラズマに保持することによって,栄養分代謝を制御します. このメカニズムは,飢餓と炭素源の調節に関連する遺伝子の発現を妨げます.
科学分野:
- 細胞生物学 細胞生物学
- 分子生物学は分子生物学である.
- バイオケミストリー バイオケミストリー
背景:
- ラパミシンの標的 (TOR) 信号伝達経路は,サッカロマイチス・セレヴィシアの窒素や炭素のような栄養素に反応して細胞の成長を調節する.
- TORキナーゼ (TOR1とTOR2) は,TAP42経由でタンパク質の合成と分解を制御するが,核イベントにおける,特に飢餓による転写抑制における,その役割は不明である.
研究 の 目的:
- TORシグナル伝達経路が核事象,特に飢餓特有の転写の抑制を制御するメカニズムを解明する.
- TORシグナリングが,窒素と炭素の可用性によって調節される遺伝子の発現にどのように影響するか調査する.
主な方法:
- TOR依存型リン酸化によって媒介されるGLN3とURE2の相互作用を調査した.
- GLN3のリン酸化と細胞プラズマの保持におけるTAP42とSIT4フォスファタゼの役割を分析した.
- TORに依存するプロセスであるMSN2とMSN4のBMH2への結合を調べました.
主要な成果:
- TORシグナリングは,URE2とGATA転写因子GLN3の結合を促進し,TOR依存型GLN3のリン酸化を必要とする.
- GLN3のリン酸化と細胞質の局所化は,TORエフェクターTAP42に依存し,フォスファターゼSIT4によって反対されます.
- TORシグナリングは,転写活性化剤MSN2とMSN4が細胞質タンパク質BMH2と結合することを強化することによって,炭素源調節遺伝子を抑制する.
結論:
- TOR信号伝達経路は,GLN3,MSN2,MSN4を含む複数の転写因子を細胞質に隔離することによって,栄養素代謝を広く調節する.
- このTORによる細胞質連鎖は,栄養素の制限と特定の炭素源に関連した遺伝子の転写を防ぐ.
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