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Register a new userThe nonlinear motion of cells subject to external forces
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To develop a minimal model for a cell moving in a crowded environment such as in tissue, we investigate the response of a liquid drop of active matter moving on a flat rigid substrate to forces applied at its boundaries. Our model incorporates active stresses due to a prescribed orientation profile of the cytoskeleton, coupling with the substrate, surface tension and imposed boundary forces. We find a highly non-linear response to forces that we characterise using the drop velocity, its shape, and the traction between the drop and the substrate. There are two main modes of motion: a long and thin drop with zero traction in the bulk, mostly occurring under strong stretching forces, and a parabolic drop with finite traction in the bulk, mostly occurring under strong squeezing forces. There is a sharp transition between these two modes as a function of the applied forces and indications of drop break-up where large forces stretch the drop in opposite directions.
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We follow the dynamics of an ensemble of interacting self-propelled semi-flexible polymers in contact with a thermal bath. We characterize structure and dynamics of the passive system and as a function of the motor activity. We find that the fluctuation-dissipation relation allows for the definition of an effective temperature that is compatible with the results obtained by using a tracer particle as a thermometer. The effective temperature takes a higher value than the temperature of the bath when the effect of the motors is not correlated with the structural rearrangements they induce. Our data are compatible with a dependence upon the square of the motor strength (normalized by the average internal force) and they suggest an intriguing linear dependence on the tracer diffusion constant times the density of the embedding matrix. We show how to use this concept to rationalize experimental results and suggest possible innovative research directions.
We elucidate the elastic behavior of a wormlike chain in 3D under compression and provide exact solutions for the experimentally accessible force-extension relation in terms of generalized spheroidal wave functions. In striking contrast to the classical Euler buckling instability, the force-extension relation of a clamped semiflexible polymer exhibits a smooth crossover from an almost stretched to a buckled configuration. In particular, the associated susceptibility, which measures the strength of the response of the polymer to the applied force, displays a prominent peak in the vicinity of the critical Euler buckling force. For increasing persistence length, the force-extension relation and the susceptibility of semiflexible polymers approach the behavior of a classical rod, whereas thermal fluctuations permit more flexible polymers to resist the applied force. Furthermore, we find that semiflexible polymers confined to 2D can oppose the applied force more strongly than in 3D.
The cell cytoskeleton is a striking example of active medium driven out-of-equilibrium by ATP hydrolysis. Such activity has been shown recently to have a spectacular impact on the mechanical and rheological properties of the cellular medium, as well as on its transport properties : a generic tracer particle freely diffuses as in a standard equilibrium medium, but also intermittently binds with random interaction times to motor proteins, which perform active ballistic excursions along cytoskeletal filaments. Here, we propose for the first time an analytical model of transport limited reactions in active media, and show quantitatively how active transport can enhance reactivity for large enough tracers like vesicles. We derive analytically the average interaction time with motor proteins which optimizes the reaction rate, and reveal remarkable universal features of the optimal configuration. We discuss why active transport may be beneficial in various biological examples: cell cytoskeleton, membranes and lamellipodia, and tubular structures like axons.
Heterogeneity is a hallmark of all cancers. Tumor heterogeneity is found at different levels -- interpatient, intrapatient, and intratumor heterogeneity. All of them pose challenges for clinical treatments. The latter two scenarios can also increase the risk of developing drug resistance. Although the existence of tumor heterogeneity has been known for two centuries, a clear understanding of its origin is still elusive, especially at the level of intratumor heterogeneity (ITH). The coexistence of different subpopulations within a single tumor has been shown to play crucial roles during all stages of carcinogenesis. Here, using concepts from evolutionary game theory and public goods game, often invoked in the context of the tragedy of commons, we explore how the interactions among subclone populations influence the establishment of ITH. By using an evolutionary model, which unifies several experimental results in distinct cancer types, we develop quantitative theoretical models for explaining data from {it in vitro} experiments involving pancreatic cancer as well as {it vivo} data in glioblastoma multiforme. Such physical and mathematical models complement experimental studies, and could optimistically also provide new ideas for the design of efficacious therapies for cancer patients.
Cell migration and mechanics are tightly regulated by the integrated activities of the various cytoskeletal networks. In cancer cells, cytoskeletal modulations have been implicated in the loss of tissue integrity, and acquisition of an invasive phenotype. In epithelial cancers, for example, increased expression of the cytoskeletal filament protein vimentin correlates with metastatic potential. Nonetheless, the exact mechanism whereby vimentin affects cell motility remains poorly understood. In this study, we measured the effects of vimentin expression on the mechano-elastic and migratory properties of the highly invasive breast carcinoma cell line MDA231. We demonstrate here that vimentin stiffens cells and enhances cell migration in dense cultures, but exerts little or no effect on the migration of sparsely plated cells. These results suggest that cell-cell interactions play a key role in regulating cell migration, and coordinating cell movement in dense cultures. Our findings pave the way towards understanding the relationship between cell migration and mechanics, in a biologically relevant context.
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