Abstract:
The architecture of the actin cortex determines the generation and transmission of stresses, during key events from cell division to migration. However, its impact on myosin-induced cell shape changes remains unclear. Here, we reconstitute a minimal model of the actomyosin cortex with branched or linear F-actin architecture within giant unilamellar vesicles (GUVs, liposomes). Upon light activation of myosin, neither the branched nor linear F-actin architecture alone induces significant liposome shape changes. The branched F-actin network forms an integrated, membrane-bound \"no-slip boundary\" -like cortex that attenuates actomyosin contractility. By contrast, the linear F-actin network forms an unintegrated \"slip boundary\" -like cortex, where actin asters form without inducing membrane deformations. Notably, liposomes undergo significant deformations at an optimized balance of branched and linear F-actin networks. Our findings highlight the pivotal roles of branched F-actin in force transmission and linear F-actin in force generation to yield membrane shape changes.
摘要:
肌动蛋白皮层的结构决定了应力的产生和传递,在从细胞分裂到迁移的关键事件中。然而,其对肌球蛋白诱导的细胞形状变化的影响尚不清楚.这里,我们重建了一个最小的肌动球蛋白皮质模型,在巨大的单层囊泡中具有分支或线性的F-肌动蛋白结构(GUV,脂质体)。肌球蛋白光激活后,单独的分支或线性F-肌动蛋白结构均不诱导显著的脂质体形状变化。分支的F-肌动蛋白网络形成一个完整的,膜结合\“无滑移边界\”样皮质,减弱肌动球蛋白收缩性。相比之下,线性F-肌动蛋白网络形成一个未整合的“滑移边界”状皮层,肌动蛋白形成而不引起膜变形。值得注意的是,脂质体在分支和线性F-肌动蛋白网络的最佳平衡下经历明显的变形。我们的发现强调了分支F-肌动蛋白在力传递和线性F-肌动蛋白在力产生中产生膜形状变化的关键作用。