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転写因子NorRの非ヘム鉄センターは,酸化窒素を感知する

Benoît D'Autréaux¹, Nicholas P Tucker, Ray Dixon

¹John Innes Centre, Colney, Norwich NR4 7UH, UK.

|September 30, 2005

まとめ

この研究は,腸内細菌が酸化窒素 (NO) をどのように感知するかを明らかにしています. NorRタンパク質は,NOを検出するためにユニークな鉄センターを使用し,保護遺伝子を活性化させ,非ヘム鉄硫黄群の新たな生物学的役割を実証しています.

科学分野:

微生物学微生物学とは
バイオケミストリーバイオケミストリー
分子生物学は分子生物学である.

背景:

酸化窒素 (NO) は,真核細胞経路と病原体防御における役割を持つ重要なシグナル伝達分子である.
病原体は,NOと活性窒素種に対抗するメカニズムを開発しています.
NOを感知する調節タンパク質は,細胞反応の鍵であり,NorRは腸内細菌におけるユニークなNO反応性転写因子である.

研究の目的:

ノルRタンパク質が酸化窒素 (NO) を感知するメカニズムを解明する.
NorRによるEscherichia coli*におけるNO検出の構造的・機能的基礎を調査する.
NorRによるNO感知が,どのように下流遺伝子の活性化につながるのかを理解する.

主な方法:

NorRの規制領域の生化学的特徴.
NO結合部位を特定するために,光譜分析を行います.
酵素活性測定はATPaseと転写活性化を測定する.
NO結合と,NorR機能に対するその影響に関するインビトロ研究.

主要な成果:

NorRの規制ドメインは,単核非ヘム鉄中心部を有する.
この鉄の中心は,酸化窒素 (NO) を反転的に結合する.
NOがNorRに結合すると,そのATPアゼの活性が活性化され,その結果, *norVW*遺伝子の転写が促進されます.

結論:

NorRは,NOセンシングのためのノンヘム鉄のセンターを採用し,新しいメカニズムを表しています.
NOの結合は,トランスクリプションの活性化につながる形状の変化を誘発する.
この発見は,NOシグナル伝達における非ヘムモノニトロシル鉄複合体の前例のない生物学的役割を強調しています.

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