通过核活塞产生分隔压力,在3D矩阵中控制细胞运动
Ryan J Petrie1, Hyun Koo2, Kenneth M Yamada1
1Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4370, USA. petrier@mail.nih.gov kyamada@mail.nih.gov.
概括
细胞的actomyosin收缩性通过创建高压突起驱动3D迁移. 核作为一个活塞,对细胞质进行细分,并增加压力,使其独立于lamellipodia的运动.
科学领域:
- 细胞生物学 细胞生物学
- 生物物理学的生物物理.
- 细胞外矩阵动力学
背景情况:
- 在三维 (3D) 环境中细胞迁移对于发育和疾病至关重要.
- 在3D迁移过程中,actomyosin收缩性会影响细胞突起类型,但机制尚不清楚.
研究的目的:
- 阐明actomyosin收缩性和核定位在驱动3D细胞迁移中的作用.
- 为了研究细胞内压力如何影响细胞在3D矩阵中迁移期间的突起形成.
主要方法:
- 利用人类细胞在3D细胞外基质中迁移.
- 操纵nesprin-3表达以评估其对核定位和细胞内压力的影响.
- 测量了细胞内压力和观察到的细胞突起动态.
主要成果:
- 在3D迁移细胞中,actomyosin收缩性产生了高压的垂突起.
- 核在物理上将细胞质分为不同的前后隔间.
- 尼斯-3调解了核定位,其减小降低了细胞内压力,并使压力分布均.
结论:
- 核的功能是活塞,对细胞质进行细分,并产生水静压,以驱动lamellipodia独立的3D细胞迁移.
- 尼斯-3在将actomyosin的收缩性与细胞核定位和细胞内压力调节的细胞移动之间起着关键作用.
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