Resolving the Mechanism of Subdiffusion in Cells

Abstract

Subdiffusion, a diffusion process characterized by a slower-than-linear increase of the mean squared displacement over time, is widely observed inside cells. However, its mechanism and origin are not well understood. To close the gap between theory and experiment, we attempt to infer the microscopic origin of subdiffusion in this thesis by simulating two biologically relevant models (a patchy-colloid network with transient interactions and a polymer network) and by analyzing the trajectories of protein condensates in chromatin networks in the human nucleus. We highlight the viscoelasticity of the chromatin networks as the primary origin of the subdiffusion but found that neither the transient networks nor the polymer networks generate sufficient viscoelasticity so that other purely-repulsive particles moving within the networks would exhibit subdiffusive behaviors in the simulation. Viscoelasticity was also shown to be connected to the confined motion of the droplets and the droplet sizes, suggesting an interplay between the droplet coarsening, the chromatin network viscoelasticity, and the subdiffusion motion.