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Intracellular transport of organelles is fundamental to cell function and health. The mounting evidence suggests that this transport is in fact anomalous. However, the reasons for the anomaly is still under debate. We examined experimental trajectories of organelles inside a living cell and propose a mathematical model that describes the previously reported transition from sub-diffusive to super-diffusive motion. In order to explain super-diffusive behaviour at long times, we introduce non-Markovian detachment kinetics of the cargo: the rate of detachment is inversely proportional to the time since the last attachment. Recently, we observed the non-Markovian detachment rate experimentally in eukaryotic cells. Here we further discuss different scenarios of how this effective non-Markovian detachment rate could arise. The non-Markovian model is successful in simultaneously describing the time-averaged variance (the time-averaged mean squared displacement corrected for directed motion), the mean first passage time of trajectories and the multiple peaks observed in the distributions of cargo velocities. We argue that non-Markovian kinetics could be biologically beneficial compared to the Markovian kinetics commonly used for modelling, by increasing the average distance the cargoes travel when a microtubule is blocked by other filaments. In turn, sub-diffusion allows cargoes to reach neighbouring filaments with higher probability, which promotes active motion along the microtubules.
Trajectories of endosomes inside living eukaryotic cells are highly heterogeneous in space and time and diffuse anomalously due to a combination of viscoelasticity, caging, aggregation and active transport. Some of the trajectories display switching
Several independent observations have suggested that catastrophe transition in microtubules is not a first-order process, as is usually assumed. Recent {it in vitro} observations by Gardner et al.[ M. K. Gardner et al., Cell {bf147}, 1092 (2011)] sho
Long cell protrusions, which are effectively one-dimensional, are highly dynamic subcellular structures. Length of many such protrusions keep fluctuating about the mean value even in the the steady state. We develop here a stochastic model motivated
We discuss the problem of proteasomal degradation of proteins. Though proteasomes are important for all aspects of the cellular metabolism, some details of the physical mechanism of the process remain unknown. We introduce a stochastic model of the p
We study stochastic copying schemes in which discrimination between a right and a wrong match is achieved via different kinetic barriers or different binding energies of the two matches. We demonstrate that, in single-step reactions, the two discrimi