分子から生物のキラリティは,保存されたミオシン1Dによって誘発される
G Lebreton1, C Géminard1, F Lapraz1
1Université Côte D'Azur, CNRS, Inserm, Institut de Biologie Valrose, Nice, France.
Science (New York, N.Y.)
|November 24, 2018
まとめ
この研究は,Drosophila myosin 1D (Myo1D) が細胞と体を歪めることで生物学的対称性を破ることを明らかにしています. この分子モーターは
科学分野:
- 発達生物学
- 細胞生物学
- バイオ物理学
背景:
- 生物学的なシステムは分子から生物まで 複数のスケールで不対称性を表しています
- これらの多層の非対称性の関係はよく理解されていません.
- シンメトリーブレイクの理解は 発達過程において極めて重要です
研究 の 目的:
- 生物系における de novo 非対称性の生成の基礎となる分子機構を調査する.
- 方向の回転に 責任のある特定の分子モーターを特定する.
- 異なる生物学的レベルでの対称性の破壊における ミオシンの役割を調査する.
主な方法:
- ドロソフィラ・メラノガスターをモデル生物として利用した.
- ミオシン1D (Myo1D) とミオシン1C (Myo1C) の細胞および生物の歪みにおける機能を調査した.
- アクチンフィラメントの滑り動態を分析する実験を in vitro で行った.
主要な成果:
- ミオシン1D (Myo1D) とミオシン1C (Myo1C) は,細胞,臓器,および全体の方向性歪みを誘導することができます.
- 歪みの方向性はミオシンモータードメインによって決定され,Myo1DとMyo1Cの間で互換性があります.
- Myo1Dはアクチン繊維の逆方向の滑り方を促進する.
結論:
- ミオシン1D (Myo1D) は,すべての生物学的スケールで対称性を破るキラル決定体として作用します.
- Myo1Dとアクチン細胞骨格の間のキラル相互作用は,新しい非対称性の基本的メカニズムです.
- これらの発見は 生物の非対称性がどのように現れるかを理解するための 分子基盤を提供します
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