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菌類によって誘発された細胞の混合は,競争的な組織侵入と破壊のために必要である
Romain Levayer1, Barbara Hauert1, Eduardo Moreno1
1Institute for Cell Biology, University of Bern, Baltzerstrasse 4, 3012 Bern, Switzerland.
Nature
|August 20, 2015
まとめ
細胞の競争を促し 組織への侵入を促します 細胞間インターケレーションと変異した細胞接合は,このプロセスにおける重要なメカニズムであり,腫瘍遺伝子の活動と病的な組織変化を結びつける.
科学分野:
- 発達生物学
- 細胞生物学
- 腫瘍学
背景:
- 細胞間インターケレーションは 発達中の組織を形作ります
- 細胞の競争により 細胞の健康状態が保たれます
- がんのような病理において,インターケレーションの役割は不明である.
研究 の 目的:
- 細胞の競争における原発がん菌の役割を調査する.
- 細胞間インターケレーションが腫瘍遺伝子の誘発による組織拡張に寄与するかどうかを判断する.
- 競争中に敗者細胞の排除の背後にあるメカニズムを解明する.
主な方法:
- ドロソフィラ・プーパ・ノータムと翼のイメージナル・ディスクにおける長期生体画像
- 細胞と細胞の接触,インターフェース形態,細胞の混合の分析.
- 微分成長,表面張力,F-アクチン,およびフォスファディチルノシトール (3,4,5) - トリフォスファートの役割を調査する.
主要な成果:
- 敗者細胞の排除確率は 勝者と敗者の接触表面積と相関する.
- 細胞同士のインターケレーションは 勝者と敗者の細胞の混合を促し 排除に不可欠です
- F-アクチンとPIP3によって調節される微分界面の緊張は,細胞の混合を促進し,クローンの密度を低下させる.
結論:
- プロトオンコゲン菌,細胞間インターケレーション,腫瘍のような拡大との関係を確立する.
- 損失細胞の除去には,インターケレーションによる細胞混合が必要であることを示します.
- 腫瘍遺伝子の誘発による細胞の競争と 組織侵襲性を引き起こします
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