FLRT粘着分子を介してニューロン移動を制御することによって,脳皮質の折り畳みを調節する
Daniel Del Toro1, Tobias Ruff1, Erik Cederfjäll1
1Max Planck Institute of Neurobiology, Am Klopferspitz 18, 82152 Martinsried, Germany.
Cell
|May 6, 2017
まとめ
FLRT1とFLRT3というニューロンの粘着分子の変化は,原始細胞の増幅ではなく,ニューロンの移動を変化させることで,哺乳類の脳皮質の折り畳みを誘導する. これは細胞間粘着が 種間の皮質の折りたたみの鍵であることを示唆しています
科学分野:
- 神経科学
- 発達生物学
- 遺伝学
背景:
- 哺乳類の脳機能には 皮質の折りたたみが不可欠です
- このプロセスは従来,プロジェニータ細胞の増幅と接触移動と関連しています.
研究 の 目的:
- 皮質の折りたたみの原因となる 分子機構を解明する
- この過程におけるニューロン移動と細胞間結合の役割を調査する.
主な方法:
- FLRT1とFLRT3の粘着分子の欠損があるマウスモデルを使用した.
- 皮質の構造,原始細胞の集団,神経細胞の移動パターンを分析した.
- 計算分析とシミュレーションを行いました
主要な成果:
- FLRT1/3の消去は,マクロスコプ的皮質の折りたたみ (sulci) を導いた.
- 皮質の折りたたみは 変異したニューロンの移動に依存し, 先祖細胞の増幅ではない.
- 細胞間粘着の減少とニューロンの移動の増加は,皮質板にクラスタリングをもたらし,硫黄の形成を促進しました.
- 低FLRT1/3発現がヒトとフレットの皮質,特に成長する部部で観察された.
結論:
- FLRT1/3によって調節される細胞間粘着は,皮質の折りたたみの重要な決定因子です.
- 粘着によって影響されるニューロン移動のダイナミクスは,脳皮質の形成に重要な役割を果たします.
- これらの発見は哺乳類種間の皮質の折りたたみの保存されたメカニズムを強調しています.
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