Foxg1は早期の皮質細胞運命を抑制する

Carina Hanashima¹, Suzanne C Li, Lijian Shen

¹Developmental Genetics Program and the Department of Cell Biology, The Skirball Institute of Biomolecular Medicine, New York University Medical Center, 540 First Avenue, New York, NY 10016, USA.

Science (New York, N.Y.)

|January 6, 2004

まとめ

転写因子Foxg1は,哺乳類の脳発達中に早期に生まれたカジャル-レッツィウスニューロンの生成を抑制する. Foxg1の喪失は,これらの重要なニューロンの過剰生産につながります.

科学分野:

神経科学は神経科学である.
発達生物学発達生物学について
遺伝学遺伝学とは

背景:

哺乳類の脳皮質生成は,原始細胞が徐々にニューロンの出力を制限することを含む.
早産児と遅産児のニューロンの運命を左右する分子メカニズムは不明である.

研究の目的:

コルチコゲネシス中の早産のニューロン生産の分子調節を調査する.
神経細胞の運命を決定するトランスクリプション因子Foxg1の役割を特定する.

主な方法:

Cajal-Retziusニューロン生産への影響を観察するために,Foxg1ゼロ変異マウスを利用しました.
Foxg1の条件付き不活性化により,特定の皮質の祖先集団で Foxg1の条件付き不活性化が行われた.

主要な成果:

Foxg1のヌル突然変異者は,皮質におけるCajal-Retziusニューロン生産の過剰を示した.
Cajal-Retzius細胞運命を抑制するためのFoxg1の構成要件は,条件付き不活性化によって実証されました.

結論:

転写因子Foxg1は,皮質形成の間にカジャル-レッツィウス細胞運命を積極的に抑制する.
早期に生まれたニューロンを生成する潜在力は,後の皮質の発達中に,積極的に抑制され,失われることはありません.

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