活動に依存するIGF-1エクソサイトーシスは,Ca2+センサシナプトタグミン-10によって制御されます
Peng Cao1, Anton Maximov, Thomas C Südhof
1Department of Molecular and Cellular Physiology, and Howard Hughes Medical Institute, Stanford University, 1050 Arastradero Rd., Palo Alto, California 94305, USA.
Cell
|April 19, 2011
まとめ
シナプトタグミン-10 (Syt10) は,カルシウムセンサーとして作用し,嗅覚球の神経細胞からインスリン型の成長因子-1 (IGF-1) の分泌を誘発する. この発見は,ニューロンにおけるカルシウム依存エクソサイトーシスの新しい経路を明らかにしています.
科学分野:
- 神経科学は神経科学である.
- 細胞生物学 細胞生物学
- 分子生物学は分子生物学である.
背景:
- シナプトタグミン (Syts) は,Syt1,Syt2,Syt7,Syt9を特徴とする,エクソサイトーシスのCa(2+) センサーとして知られています.
- Syt10を含む他のSytファミリーのメンバーがエクソサイトーシスで果たす役割は,ほとんど不明のままである.
研究 の 目的:
- 嗅覚球の神経細胞におけるSyt10の機能を調査する.
- 活動に依存したIGF-1分泌に責任のあるCa2+) センサーを特定する.
主な方法:
- 遺伝子削除 (ノックアウト) と外因的なIGF-1救済を使用して,嗅覚球の神経細胞におけるSyt10の役割を調査しました.
- Syt10のIGF-1による局所化が,体質帯状膀で試験された.
- Syt10.によって誘発されたIGF-1のCa(2+) 依存エクソサイトーシスを研究した.
主要な成果:
- 嗅覚球の神経細胞は,活動に依存するエクソサイトーシス経路経由でIGF-1を分泌する.
- Syt10は,これらのニューロンにおけるIGF-1エクソサイトーシスのCa(2+) センサとして機能する.
- Syt10の消去は,より小さなニューロン,シナプスの数の減少,および外因的なIGF-1によって逆転されたIGF-1分泌の低下をもたらしました.
- Syt10は膀内のIGF-1とコロカライズされ,Ca ((2+) 誘発のIGF-1分泌を媒介する.
結論:
- Syt10は,嗅覚球の神経細胞におけるIGF-1のための新しい,これまで認識されていないCa(2+) に依存するエクソサイトーシス経路を調節する.
- このSyt10媒介経路は,Syt1制御のシナプス胞外細胞症とは異なる.
- ニューロンは異なるシナプトタグミンを利用して,機能的に分離したCa2+に依存した膜融合現象を調節することができます.
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