PDF(Pubmed)
Abstract：
Cytokinesis is the process where the mother cell\'s cytoplasm separates into daughter cells. This is driven by an actomyosin contractile ring that produces cortical contractility and drives cleavage furrow ingression, resulting in the formation of a thin intercellular bridge. While cytoskeletal reorganization during cytokinesis has been extensively studied, less is known about the spatiotemporal dynamics of the plasma membrane. Here, we image and model plasma membrane lipid and protein dynamics on the cell surface during leukemia cell cytokinesis. We reveal an extensive accumulation and folding of the plasma membrane at the cleavage furrow and the intercellular bridge, accompanied by a depletion and unfolding of the plasma membrane at the cell poles. These membrane dynamics are caused by two actomyosin-driven biophysical mechanisms: the radial constriction of the cleavage furrow causes local compression of the apparent cell surface area and accumulation of the plasma membrane at the furrow, while actomyosin cortical flows drag the plasma membrane toward the cell division plane as the furrow ingresses. The magnitude of these effects depends on the plasma membrane fluidity, cortex adhesion, and cortical contractility. Overall, our work reveals cell-intrinsic mechanical regulation of plasma membrane accumulation at the cleavage furrow that is likely to generate localized differences in membrane tension across the cytokinetic cell. This may locally alter endocytosis, exocytosis, and mechanotransduction, while also serving as a self-protecting mechanism against cytokinesis failures that arise from high membrane tension at the intercellular bridge.
摘要：
细胞分裂是母细胞的细胞质分离成子细胞的过程。这是由肌动球蛋白收缩环驱动的，该环产生皮质收缩性并驱动卵裂沟侵入，导致形成薄的细胞间桥。虽然胞质分裂过程中的细胞骨架重组已经得到了广泛的研究，对质膜的时空动力学知之甚少。这里,我们对白血病细胞胞质分裂过程中细胞表面的质膜脂质和蛋白质动力学进行成像和建模。我们揭示了在卵裂沟和细胞间桥的质膜的广泛积累和折叠，伴随着细胞极处质膜的耗尽和展开。这些膜动力学是由两种肌动球蛋白驱动的生物物理机制引起的：分裂沟的径向收缩导致表观细胞表面积的局部压缩和质膜在沟中的积累，而肌动球蛋白皮质流将质膜拖向细胞分裂平面，因为沟进入。这些影响的大小取决于质膜的流动性，皮层粘连,和皮质收缩性。总的来说,我们的工作揭示了分裂沟质膜积累的细胞内在机械调节,这可能在整个细胞动力学细胞中产生局部的膜张力差异.这可能会局部改变内吞作用，胞吐作用,和机械传导，同时也作为一种自我保护机制，以抵抗由于细胞间桥的高膜张力而引起的胞质分裂失败。
