ABSTRACT
Microrheology is a powerful tool to investigate the mechanical properties of living cells, which are essential to many biological functions such as cellular adhesion, migration, and division. After a synthetic presentation of rheology basics for complex systems, we describe the optical tweezers and the uniaxial stretching techniques, which allow us to probe the microrheology of individual cells at different length scales and over a wide time range. The creep function J (t) and viscoelastic modulus Ge() are retrieved from both experiments and always exhibit weak power law behaviors as functions of time and frequency, respectively. The exponent ≈ 0.2 of this power law appears very robust and shows almost no dependence on the cell type, nor on the typical length scale of the experiment. On the contrary, the typical rigidity of the cells, characterized for instance by the viscoelastic modulus G0 at 1 Hz, varies over almost two orders of magnitude from one cell type to another. We propose an interpretation of the observed power law rheology, based on a semi-phenomenological model involving a scale-free structure of the cellular network and a broad and dense distribution of relaxation times in the system. This model leads to power law mechanical responses and accurately predicts the normal distribution of the exponent and the log-normal distribution of G0, as experimentally observed.
Eukaryotic cells and intracellular pathogens such as bacteria or viruses utilize the actin polymerization machinery to propel themselves forward. Thereby, the onset of motion and choice of direction may be the result of a spontaneous symmetry breaking or might be triggered by external signals and preexisting asymmetries, for example, through a previous septation in bacteria. Although very complex, a key feature of cellular motility is the ability of actin to form dense polymeric networks, whose microstructures are tightly regulated by the cell. These polar actin networks produce the forces necessary for propulsion but may also be at the origin of a spontaneous symmetry breaking. Understanding the exact role of actin dynamics in cell motility requires multiscale approaches that capture at the same time the polymer network structure and dynamics on the scale of a few nanometers and the macroscopic distribution of elastic stresses on the scale of the whole cell. In this chapter we review a selection of theories on how mechanical material properties and growth processes interact to induce the onset of actin-based motion.
