耦合的细胞膜-细胞骨架的相变改变细胞形状。
Phase transitions of the coupled membrane-cytoskeleton modify cellular shape.
作者信息
Veksler Alex, Gov Nir S
机构信息
Department of Chemical Physics, The Weizmann Institute of Science, Rehovot, Israel.
出版信息
Biophys J. 2007 Dec 1;93(11):3798-810. doi: 10.1529/biophysj.107.113282. Epub 2007 Aug 17.
Formation of protrusions and protein segregation on the membrane is of a great importance for the functioning of the living cell. This is most evident in recent experiments that show the effects of the mechanical properties of the surrounding substrate on cell morphology. We propose a mechanism for the formation of membrane protrusions and protein phase separation, which may lay behind this effect. In our model, the fluid cell membrane has a mobile but constant population of proteins with a convex spontaneous curvature. Our basic assumption is that these membrane proteins represent small adhesion complexes, and also include proteins that activate actin polymerization. Such a continuum model couples the membrane and protein dynamics, including cell-substrate adhesion and protrusive actin force. Linear stability analysis shows that sufficiently strong adhesion energy and actin polymerization force can bring about phase separation of the membrane protein and the appearance of protrusions. Specifically, this occurs when the spontaneous curvature and aggregation potential alone (passive system) do not cause phase separation. Finite-size patterns may appear in the regime where the spontaneous curvature energy is a strong factor. Different instability characteristics are calculated for the various regimes, and are compared to various types of observed protrusions and phase separations, both in living cells and in artificial model systems. A number of testable predictions are proposed.
膜上突起的形成和蛋白质分离对于活细胞的功能至关重要。这在最近的实验中最为明显,这些实验展示了周围基质的力学性质对细胞形态的影响。我们提出了一种膜突起形成和蛋白质相分离的机制,这可能是这种影响背后的原因。在我们的模型中,流体细胞膜具有一群具有凸自发曲率的可移动但数量恒定的蛋白质。我们的基本假设是这些膜蛋白代表小的粘附复合物,并且还包括激活肌动蛋白聚合的蛋白质。这样一个连续介质模型将膜和蛋白质动力学耦合在一起,包括细胞 - 基质粘附和突出的肌动蛋白力。线性稳定性分析表明,足够强的粘附能和肌动蛋白聚合力可以导致膜蛋白的相分离和突起的出现。具体来说,当仅自发曲率和聚集势(无源系统)不会导致相分离时,就会发生这种情况。在自发曲率能是一个重要因素的区域可能会出现有限尺寸图案。针对各种区域计算了不同的不稳定性特征,并与活细胞和人工模型系统中观察到的各种类型的突起和相分离进行了比较。提出了一些可检验的预测。