焦点粘附衍生的液体-液体相分离调节mRNA翻译.
Abhishek Kumar1, Keiichiro Tanaka1, Martin A Schwartz1,2,3
1Yale Cardiovascular Research Center, Department of Internal Medicine (Division of Cardiovascular Medicine), 300 George St. New Haven CT 06511.
bioRxiv : the preprint server for biology
|December 4, 2023
概括
细胞粘附蛋白p130Cas驱动液-液相分离 (LLPS) 凝结物,抑制mRNA转化. 这种新的机制将细胞粘附强度与蛋白质合成调节联系起来,影响细胞状态,如静止.
科学领域:
- 细胞生物学 细胞生物学
- 生物化学 生物化学
- 分子生物学分子生物学
背景情况:
- 液-液相分离 (LLPS) 是细胞组织的一个关键原则.
- 众所周知,因特林介导的焦点粘附和像p130Cas这样的蛋白质会经历LLPS.
- 焦点粘附中的LLPS影响细胞粘附动态和行为.
研究的目的:
- 研究p130Cas在形成具有LLPS特征的细胞质结构中的作用.
- 为了确定这些p130Cas凝聚物是否调节mRNA翻译.
- 阐明一种将细胞粘附与翻译控制联系起来的新机制.
主要方法:
- 在p130Cas涂层珠子周围诱导LLPS类结构.
- 隔离和分析这些凝结物的组成.
- 使用高度的纤维内素来诱导大焦点粘附.
- 采用光感应式Cry2系统进行凝结体的感应.
- 测量mRNA转化率,以应对这些条件.
主要成果:
- p130Cas驱动着从焦点粘附中芽的LLPS类结构的形成.
- 这些凝结物富含着焦点粘附蛋白,mRNA和RNA结合蛋白,包括翻译抑制剂.
- 高度的纤维内素诱导焦点粘附,抑制mRNA转化,依赖p130Cas,与滴滴形成相关.
- 对p130Cas凝聚物的光诱导也减少了翻译.
结论:
- 确定了一个新的调节机制,其中高细胞粘附限制了通过p130Cas依赖的细胞质LLPS的mRNA转换.
- 这种机制可能解释了强粘性肌纤维细胞和衰老细胞中观察到的静止状态.
- 卡斯驱动的LLPS作为细胞粘附和转化控制之间的关键环节.
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