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アクソナルタンパク質合成は,中間標的の局所的な調節のためのメカニズムを提供します

Perry A Brittis¹, Qiang Lu, John G Flanagan

¹Department of Cell Biology and Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA.

|August 2, 2002

まとめ

アクソンは局所的にタンパク質を合成し,EphA2アップレギュレーションのような受容体の変化を可能にします. このRNAベースのメカニズムは,神経発達中の特定の軸索セグメント内の標的タンパク質発現を可能にします.

科学分野:

神経科学は神経科学である.
分子生物学は分子生物学である.
発達生物学発達生物学とは

背景:

軸索は,成長するにつれて,誘導シグナル応答性を変化させます.
局所的受容体発現の変化が関与しているが,そのメカニズムは不明である.

研究の目的:

地元のタンパク質合成とアクソンの受容体のアップレギュレーションのメカニズムを調査する.
軸索が局所翻訳と細胞表面タンパク質発現のための機械を持っているかどうかを判断する.

主な方法:

視覚化可能なレポーターRNAは,個々の切断された軸索と成長に導入されました.
タンパク質合成と細胞表面輸出が追跡された.
レポーターアップレギュレーションにおけるEphA2 mRNA 3' 未翻訳領域の役割を調べました.

主要な成果:

個々の軸索と成長は,タンパク質翻訳と輸出の能力を示した.
EphA2受容体は,脊髄の中央線付近の遠端アクソンセグメントで上調されていることが判明しました.
EphA2 mRNA 3' 未翻訳領域の保存された領域は,このミッドラインレポーターのアップレギュレーションを再現した.

結論:

アクソンは,局所的なタンパク質合成と細胞表面発現のための固有の機械を有しています.
潜在的にEphA2 mRNA 3' UTRを含むRNAベースのメカニズムは,特定の軸索亜領域内のタンパク質発現を調節する.
これは,発達中の軸索応答性の動的制御のための柔軟なメカニズムを提供します.

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