网状粘附在平坦的克拉特林格子上组装在一起,并与活性整合素α5β1对立
Laura Hakanpää1,2,3, Amr Abouelezz1,2,3, An-Sofie Lenaerts1,2,3
1Helsinki Institute of Life Science, University of Helsinki , Helsinki, Finland.
The Journal of cell biology
|May 26, 2023
概括
网状粘附 (RAs) 聚集在平坦的克拉特林格子 (FCLs) 上,挑战了内细胞分裂只会分解细胞粘附的观点. 这种新的机制涉及纤维素和整蛋白信号传递,影响细胞迁移.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 网状粘附体 (RAs) 含有整合素αvβ5和平面克拉特林格子 (FCLs).
- FCL与克拉斯林介导的内细胞瘤 (CME) 载体共享分子成分,但FCL和RA的同位化尚不清楚.
- 传统的理解是,内细胞分裂分解细胞粘附.
研究的目的:
- 为了阐明网状粘附组件的机制.
- 调查FCL,CME和RA形成之间的关系.
- 探索纤维素和其受体在RA组合和细胞迁移中的作用.
主要方法:
- 在富含纤维菌素 (FN) 的基质上培养细胞.
- 克拉特林介导的内分细胞分裂 (CME) 机制的抑制.
- 活细胞成像观察RA建立和FCL联合组装.
- 在Tensin1-阳性纤维状粘附中分析整合素α5β1激活.
主要成果:
- 网状粘附 (RAs) 在平面克拉特林格子 (FCLs) 上聚集.
- 纤维蛋白 (FN) 和整体蛋白α5β1控制RA组件.
- 抑制CME机器废除RA,表明FCL联合组装是RA建立所需的.
- 在RA上FN的抑制活性是由纤维状粘附处的整合素α5β1激活的介导.
- 一个新的机制显示了内细胞蛋白积极组装细胞粘附.
结论:
- 内细胞蛋白,特别是FCL的组成部分,积极参与像RA这样的细胞粘附的组装.
- 这种新型的粘附组装机制与通过与细胞矩阵粘附的交叉通道的细胞迁移有关.
- 这些发现挑战了传统的看法,认为内细胞分裂仅仅是细胞粘附的拆卸过程.
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