核のCa2+貯蔵庫の枯渇によって引き起こされる核毛孔複合体の形状状態

C Perez-Terzic¹, J Pyle, M Jaconi

¹Department of Pharmacology, Mayo Foundation, Rochester, MN 55905, USA.

Science (New York, N.Y.)

|September 27, 1996

まとめ

カルシウムのレベルは,細胞輸送のゲートキーパーである核孔複合体 (NPC) を調節します. 枯渇したカルシウムは,NPCの詰まりを引き起こし,分子通過を遮断し,ゲーティング機能を明らかにします.

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.
バイオフィジックス生物物理学

背景:

核孔複合体 (NPC) は,細胞質と核質の間の分子輸送を容易にする.
以前は,NPCは10,000Daまでの分子の自由な拡散を可能にすると信じられていた.
核包膜の透過性におけるカルシウムの役割は,ほとんど未研究であった.

研究の目的:

核毛孔複合体 (NPC) 機能を調節するカルシウムの役割を調査する.
カルシウム濃度に応じてNPCの形状が変化するかどうかを判断する.
NPCが分子輸送を制御するメカニズムを解明する.

主な方法:

NPC構造の高解像度イメージングのためのフィールドエミッションスキャニング電子顕微鏡 (FESEM).
原子力顕微鏡 (AFM) で,NPCの表面地形と形状の変化を調査する.
Xenopus laevisの卵細胞は,核包膜の浸透性を研究するためのモデルシステムである.

主要な成果:

核カルシウムの枯渇は,中等サイズの分子の制御された通過と相関していた.
NPCの2つの異なる構成状態が視覚化されました.
カルシウムの枯渇に伴い,NPCチャネル内の中央プラグ形成が観察され,拡散を阻害しました.

結論:

NPCの形状は,細胞内カルシウムレベルによって動的に調節されます.
NPCはダイナミック・ゲートとして機能し,核の封筒にわたる分子交通を制御する.
カルシウムの枯渇は,閉ざされたNPC状態を誘導し,中間型の分子の自由な拡散を防ぐ.

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