電子再プログラムによる微生物ロドプシンの光増強

María Del Carmen Marín^1,2, Damianos Agathangelou³, Yoelvis Orozco-Gonzalez^2,4

¹Biotechnology, Pharmacy and Chemistry Department , University of Siena , Siena 53100 , Italy.

Journal of the American Chemical Society

|December 12, 2018

まとめ

光遺伝学のために微生物のロドプシンを設計し逆の光を持つ変異体を発見しました一つの変異体は赤光放射を 10倍に増幅し光増強メカニズムに洞察力を与えます

科学分野:

バイオ物理学
分子生物学
オプトジェネティクス

背景:

微生物のロドプシンが光遺伝学の重要なツールです
光性を高めるためのこれらのタンパク質の設計は重要な研究分野です.
光調節の背後にあるメカニズムの理解は,新しい光遺伝的探査機の開発に不可欠です.

研究の目的:

微生物のロドプシンを変化した光特性で設計する
感受性ロドプシンにおける光増強の分子基礎を調査する.
オプトジェネティクスの応用のためのエンジニアリングされたロドプシンの可能性を探求する.

主な方法:

アナベナPCC7120からの感知性ロドプシンのサイト指向型変異.
暫定吸収スペクトロスコーピーを含むスペクトロスコーピーの分析
マルチコンフィギュレーションの量子化学計算

主要な成果:

2つの変異体,W76S/Y179FとL83Qは,相反する光行動と特定されました.
W76S/Y179F変異体は野生型と比較して赤光放射が10倍近く増加した.
L83Q変異体は放射性でないことが判明した.
イソメリゼーションを阻害する電子効果が,サブピコ秒の光増強の原因と特定された.

結論:

W76S/Y179F,L83Q変異ペアは,微生物ロドプシンにおける光増強を研究するためのユニークなシステムを提供します.
この発見は,イソメリゼーション阻害に関連した急速な光増強のメカニズムを明らかにする.
この研究は,光遺伝学のための先進的な光探査機の開発を進めています.

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