Molecular motors transporting cargos in viscoelastic cytosol: how to beat subdiffusion with a power stroke?

Anomalously slow passive diffusion, $\langle \delta x^2(t)\rangle\simeq t^{\alpha}$, with $0<\alpha<1$, of larger tracers such as messenger RNA and endogenous submicron granules in the cytoplasm of living biological cells has been demonstrated in a number of experiments and has been attributed to the viscoelastic physical nature of the cellular cytoplasm. This finding provokes the question to which extent active intracellular transport is affected by this viscoelastic environment: does the subdiffusion of free submicron cargo such as vesicles and organelles always imply anomalously slow transport by molecular motors such as kinesins, that is, directed transport characterized by a sublinear growth of the mean distance, $\langle x(t)\rangle\simeq t^{\alpha_{\rm eff}}$, with $0<\alpha_{\rm eff}<1$? Here we study a generic model approach combining the commonly accepted two-state Brownian ratchet model of kinesin motors based on the continuous-state diffusion along microtubule driven by a flashing binding potential. The motor is elastically coupled to a cargo particle, which in turn is subject to the viscoelastic cytoplasmic environment. Depending on the physical parameters of cargo size, loading force, amplitude of the binding potential, and the turnover frequency of the molecular motor, the transport can be both normal ($\alpha_{\rm eff}=1$) and anomalous ($\alpha\leq \alpha_{\rm eff}<1$). In particular, we demonstrate in detail how highly efficient normal motor transport can emerge despite the anomalously slow passive diffusion of cargo particles, and how the active motion of the same motor in the same cell may turn anomalously slow when the parameters are changed.