Laboratory for Physical Biology, RIKEN Quantitative Biology Center, Kobe 650-0047, Japan.
Institute of Physics, Academia Sinica, Taipei 11529, Taiwan, R.O.C.
Phys Rev E. 2016 Jun;93(6):062405. doi: 10.1103/PhysRevE.93.062405. Epub 2016 Jun 3.
Actin polymerization is ubiquitously utilized to power the locomotion of eukaryotic cells and pathogenic bacteria in living systems. Inevitably, actin polymerization and depolymerization proceed in a fluctuating environment that renders the locomotion stochastic. Previously, we have introduced a deterministic model that manages to reproduce actin-propelled trajectories in experiments, but not to address fluctuations around them. To remedy this, here we supplement the deterministic model with noise terms. It enables us to compute the effects of fluctuating actin density and forces on the trajectories. Specifically, the mean-squared displacement (MSD) of the trajectories is computed and found to show a super-ballistic scaling with an exponent 3 in the early stage, followed by a crossover to a normal, diffusive scaling of exponent 1 in the late stage. For open-end trajectories such as straights and S-shaped curves, the time of crossover matches the decay time of orientational order of the velocities along trajectories, suggesting that it is the spreading of velocities that leads to the crossover. We show that the super-ballistic scaling of MSD arises from the initial, linearly increasing correlation of velocities, before time translational symmetry is established. When the spreading of velocities reaches a steady state in the long-time limit, short-range correlation then yields a diffusive scaling in MSD. In contrast, close-loop trajectories like circles exhibit localized periodic motion, which inhibits spreading. The initial super-ballistic scaling of MSD arises from velocity correlation that both linearly increases and oscillates in time. Finally, we find that the above statistical features of the trajectories transcend the nature of noises, be it additive or multiplicative, and generalize to other self-propelled systems that are not necessarily actin based.
肌动蛋白聚合普遍用于为真核细胞和生活系统中的病原细菌的运动提供动力。不可避免的是,肌动蛋白的聚合和去聚合在一个波动的环境中进行,这使得运动具有随机性。此前,我们已经引入了一个确定性模型,该模型能够在实验中再现肌动蛋白驱动的轨迹,但无法解决它们周围的波动问题。为了解决这个问题,我们在这里用噪声项来补充这个确定性模型。它使我们能够计算波动的肌动蛋白密度和力对轨迹的影响。具体来说,我们计算了轨迹的均方根位移(MSD),并发现它在早期表现出超弹道标度,指数为 3,随后在后期交叉到正常的扩散标度,指数为 1。对于开放式轨迹,如直线和 S 形曲线,交叉时间与轨迹上速度的方向有序度的衰减时间匹配,这表明是速度的扩散导致了交叉。我们表明,MSD 的超弹道标度源于速度的初始线性增加相关性,在此之前,时间平移对称性尚未建立。当速度的扩散在长时间限制下达到稳定状态时,短程相关性则导致 MSD 中的扩散标度。相比之下,像圆这样的闭环轨迹表现出局部周期性运动,这抑制了扩散。MSD 的初始超弹道标度源于线性增加和随时间振荡的速度相关性。最后,我们发现轨迹的上述统计特征超越了噪声的性质,无论是加性噪声还是乘性噪声,并推广到其他不一定基于肌动蛋白的自推进系统。