Bussell S J, Koch D L, Hammer D A
School of Chemical Engineering, Cornell University, Ithaca, New York 14853, USA.
Biophys J. 1995 May;68(5):1836-49. doi: 10.1016/S0006-3495(95)80360-7.
Tracer diffusion coefficients of integral membrane proteins (IMPs) in intact plasma membranes are often much lower than those found in blebbed, organelle, and reconstituted membranes. We calculate the contribution of hydrodynamic interactions to the tracer, gradient, and rotational diffusion of IMPs in plasma membranes. Because of the presence of immobile IMPs, Brinkman's equation governs the hydrodynamics in plasma membranes. Solutions of Brinkman's equation enable the calculation of short-time diffusion coefficients of IMPs. There is a large reduction in particle mobilities when a fraction of them is immobile, and as the fraction increases, the mobilities of the mobile particles continue to decrease. Combination of the hydrodynamic mobilities with Monte Carlo simulation results, which incorporate excluded area effects, enable the calculation of long-time diffusion coefficients. We use our calculations to analyze results for tracer diffusivities in several different systems. In erythrocytes, we find that the hydrodynamic theory, when combined with excluded area effects, closes the gap between existing theory and experiment for the mobility of band 3, with the remaining discrepancy likely due to direct obstruction of band 3 lateral mobility by the spectrin network. In lymphocytes, the combined hydrodynamic-excluded area theory provides a plausible explanation for the reduced mobility of sIg molecules induced by binding concanavalin A-coated platelets. However, the theory does not explain all reported cases of "anchorage modulation" in all cell types in which receptor mobilities are reduced after binding by concanavalin A-coated platelets. The hydrodynamic theory provides an explanation of why protein lateral mobilities are restricted in plasma membranes and why, in many systems, deletion of the cytoplasmic tail of a receptor has little effect on diffusion rates. However, much more data are needed to test the theory definitively. We also predict that gradient and tracer diffusivities are the same to leading order. Finally, we have calculated rotational diffusion coefficients in plasma membranes. They decrease less rapidly than translational diffusion coefficients with increasing protein immobilization, and the results agree qualitatively with the limited experimental data available.
完整质膜中整合膜蛋白(IMPs)的示踪扩散系数通常远低于在泡状膜、细胞器膜和重构膜中测得的扩散系数。我们计算了流体动力学相互作用对质膜中IMPs的示踪、梯度和旋转扩散的贡献。由于存在固定不动的IMPs,布林克曼方程支配着质膜中的流体动力学。布林克曼方程的解能够计算IMPs的短时间扩散系数。当一部分粒子固定不动时,粒子迁移率会大幅降低,并且随着这部分比例的增加,可移动粒子的迁移率会持续下降。将流体动力学迁移率与包含排除体积效应的蒙特卡罗模拟结果相结合,能够计算长时间扩散系数。我们利用计算结果分析了几种不同系统中示踪扩散率的实验结果。在红细胞中,我们发现流体动力学理论与排除体积效应相结合时,缩小了现有理论与带3迁移率实验结果之间的差距,剩余的差异可能是由于血影蛋白网络对带3横向迁移的直接阻碍。在淋巴细胞中,流体动力学 - 排除体积联合理论为结合伴刀豆球蛋白A包被的血小板后sIg分子迁移率降低提供了合理的解释。然而,该理论并不能解释所有报道的伴刀豆球蛋白A包被的血小板结合后受体迁移率降低的“锚定调节”情况。流体动力学理论解释了为什么蛋白质在质膜中的横向迁移受到限制,以及为什么在许多系统中,受体细胞质尾巴的缺失对扩散速率影响很小。然而,还需要更多数据来最终验证该理论。我们还预测梯度扩散率和示踪扩散率在主导阶是相同的。最后,我们计算了质膜中的旋转扩散系数。随着蛋白质固定化程度的增加,它们的下降速度比平动扩散系数慢,并且结果在定性上与现有的有限实验数据一致。