Membrane bending is a ubiquitous cellular process that is required for membrane traffic, cell motility, organelle biogenesis, and cell division. Proteins that bind to membranes using specific structural features, such as wedge-like amphipathic helices and crescent-shaped scaffolds, are thought to be the primary drivers of membrane bending. However, many membrane-binding proteins have substantial regions of intrinsic disorder, which lack a stable three-dimensional structure. Interestingly, many of these disordered domains have recently been found to form networks stabilized by weak, multi-valent contacts, leading to assembly of protein liquid phases on membrane surfaces. Here we ask how membrane-associated protein liquids impact membrane curvature. We find that protein phase separation on the surfaces of synthetic and cell-derived membrane vesicles creates a substantial compressive stress in the plane of the membrane. This stress drives the membrane to bend inward, creating protein-lined membrane tubules. A simple mechanical model of this process accurately predicts the experimentally measured relationship between the rigidity of the membrane and the diameter of the membrane tubules. Discovery of this mechanism, which may be relevant to a broad range of cellular protrusions, illustrates that membrane remodeling is not exclusive to structured scaffolds, but can also be driven by the rapidly emerging class of liquid-like protein networks that assemble at membranes.

中文翻译：

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蛋白质相分离引起的膜弯曲

膜弯曲是膜运输，细胞运动，细胞器生物发生和细胞分裂所必需的普遍存在的细胞过程。使用特定结构特征（例如楔形两亲螺旋和新月形支架）与膜结合的蛋白质被认为是膜弯曲的主要驱动力。然而，许多膜结合蛋白具有实质性的固有紊乱区域，其缺乏稳定的三维结构。有趣的是，最近发现许多这些无序域形成了通过弱的多价接触而稳定的网络，从而导致蛋白质液相在膜表面上的组装。在这里，我们问与膜相关的蛋白质液体如何影响膜曲率。我们发现合成和细胞衍生的膜囊泡表面上的蛋白质相分离会在膜平面内产生大量的压应力。这种压力驱使膜向内弯曲，形成了衬有蛋白质的膜小管。此过程的简单机械模型可准确预测膜的刚度与膜小管直径之间的实验测量关系。该机制的发现可能与广泛的细胞突起有关，这说明膜重塑不仅是结构化支架所独有的，而且还可以由在膜上组装的快速出现的类液体蛋白网络驱动。产生内衬蛋白质的膜小管。此过程的简单机械模型可准确预测膜的刚度与膜小管直径之间的实验测量关系。该机制的发现可能与广泛的细胞突起有关，这说明膜重塑不仅是结构化支架所独有的，而且还可以由在膜上组装的快速出现的类液体蛋白网络驱动。产生内衬蛋白质的膜小管。此过程的简单机械模型可准确预测膜的刚度与膜小管直径之间的实验测量关系。该机制的发现可能与广泛的细胞突起有关，这说明膜重塑不仅是结构化支架所独有的，而且还可以由在膜上组装的快速出现的类液体蛋白网络驱动。