Equilibrium physics breakdown reveals the active nature of red blood cell flickering
Equilibrium physics breakdown reveals the active nature of red blood cell flickering
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DOI：
10.1038/nphys3621
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发表时间：
2016-05-01
期刊：
影响因子：
19.6
通讯作者：
Betz, T.
中科院分区：
文献类型：
--
作者：
Turlier, H.;Fedosov, D. A.;Betz, T.
在光学显微镜下可以看到红细胞闪烁，这种现象最初被描述为细胞膜的热波动。但最近的研究表明存在非平衡过程，但没有明确排除平衡解释。使用主动和被动微流变学直接比较单个红细胞的膜响应和波动，我们在这里报告了波动耗散关系的违反，这是闪烁的非平衡性质的直接证明。通过复合红细胞膜的分析模型和现实的随机模拟，我们表明几种分子机制可以解释主动波动，并预测它们的动力学。我们证明，由血影蛋白（一种细胞骨架蛋白）形成的网络中的切向代谢活动可以产生曲率介导的主动膜运动。我们还表明，由直接法向力偶极子代表的其他活性膜过程可以解释观察到的膜活性。我们的研究结果为未来研究细胞主动运动的起源和功能提供了坚实的实验和理论框架。
Red blood cells, or erythrocytes, are seen to flicker under optical microscopy, a phenomenon initially described as thermal fluctuations of the cell membrane. But recent studies have suggested the involvement of non-equilibrium processes, without definitively ruling out equilibrium interpretations. Using active and passive microrheology to directly compare the membrane response and fluctuations on single erythrocytes, we report here a violation of the fluctuation-dissipation relation, which is a direct demonstration of the non-equilibrium nature of flickering. With an analytical model of the composite erythrocyte membrane and realistic stochastic simulations, we show that several molecular mechanisms may explain the active fluctuations, and we predict their kinetics. We demonstrate that tangential metabolic activity in the network formed by spectrin, a cytoskeletal protein, can generate curvature-mediated active membrane motions. We also show that other active membrane processes represented by direct normal force dipoles may explain the observed membrane activity. Our findings provide solid experimental and theoretical frameworks for future investigations of the origin and function of active motion in cells.