Continuous membrane-cytoskeleton adhesion requires continuous accommodation to lipid and cytoskeleton dynamics.

Michael P Sheetz, Julia E Sable, Hans-Günther Döbereiner
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引用次数: 272

Abstract

The plasma membrane of most animal cells conforms to the cytoskeleton and only occasionally separates to form blebs. Previous studies indicated that many weak interactions between cytoskeleton and the lipid bilayer kept the surfaces together to counteract the normal outward pressure of cytoplasm. Either the loss of adhesion strength or the formation of gaps in the cytoskeleton enables the pressure to form blebs. Membrane-associated cytoskeleton proteins, such as spectrin and filamin, can control the movement and aggregation of membrane proteins and lipids, e.g., phosphoinositol phospholipids (PIPs), as well as blebbing. At the same time, lipids (particularly PIPs) and membrane proteins affect cytoskeleton and signaling dynamics. We consider here the roles of the major phosphatidylinositol-4,5-diphosphate (PIP2) binding protein, MARCKS, and PIP2 levels in controlling cytoskeleton dynamics. Further understanding of dynamics will provide important clues about how membrane-cytoskeleton adhesion rapidly adjusts to cytoskeleton and membrane dynamics.

连续的膜-细胞骨架粘附需要持续适应脂质和细胞骨架动力学。
大多数动物细胞的质膜与细胞骨架一致,只是偶尔分离形成泡。先前的研究表明,细胞骨架和脂质双分子层之间的许多弱相互作用使表面保持在一起,以抵消细胞质的正常向外压力。要么是粘附强度的丧失,要么是在细胞骨架中形成间隙,从而使压力形成气泡。膜相关的细胞骨架蛋白,如谱蛋白和丝蛋白,可以控制膜蛋白和脂质的运动和聚集,如磷酸肌醇磷脂(PIPs),以及起泡。同时,脂质(尤其是pip)和膜蛋白影响细胞骨架和信号动力学。我们在此考虑了主要磷脂酰肌醇-4,5-二磷酸(PIP2)结合蛋白、MARCKS和PIP2水平在控制细胞骨架动力学中的作用。对动力学的进一步理解将提供关于膜-细胞骨架粘附如何快速适应细胞骨架和膜动力学的重要线索。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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