No Arabic abstract
We report analytical and numerical modelling of active elastic networks, motivated by experiments on crosslinked actin networks contracted by myosin motors. Within a broad range of parameters, the motor-driven collapse of active elastic networks leads to a critical state. We show that this state is qualitatively different from that of the random percolation model. Intriguingly, it possesses both euclidean and scale-free structure with Fisher exponent smaller than $2$. Remarkably, an indistinguishable Fisher exponent and the same euclidean structure is obtained at the critical point of the random percolation model after absorbing all enclaves into their surrounding clusters. We propose that in the experiment the enclaves are absorbed due to steric interactions of network elements. We model the network collapse, taking into account the steric interactions. The model shows how the system robustly drives itself towards the critical point of the random percolation model with absorbed enclaves, in agreement with the experiment.
A long standing puzzle in the rheology of living cells is the origin of the experimentally observed long time stress relaxation. The mechanics of the cell is largely dictated by the cytoskeleton, which is a biopolymer network consisting of transient crosslinkers, allowing for stress relaxation over time. Moreover, these networks are internally stressed due to the presence of molecular motors. In this work we propose a theoretical model that uses a mode-dependent mobility to describe the stress relaxation of such prestressed transient networks. Our theoretical predictions agree favorably with experimental data of reconstituted cytoskeletal networks and may provide an explanation for the slow stress relaxation observed in cells.
Animal cells form contractile structures to promote various functions, from cell motility to cell division. Force generation in these structures is often due to molecular motors such as myosin that require polar substrates for their function. Here, we propose a motor-free mechanism that can generate contraction in biopolymer networks without the need for polarity. This mechanism is based on active binding/unbinding of crosslinkers that breaks the principle of detailed balance, together with the asymmetric force-extension response of semiflexible biopolymers. We find that these two ingredients can generate steady state contraction via a non-thermal, ratchet-like process. We calculate the resulting force-velocity relation using both coarse-grained and microscopic models.
Myosin motor proteins drive vigorous steady-state fluctuations in the actin cytoskeleton of cells. Endogenous embedded semiflexible filaments such as microtubules, or added filaments such as single-walled carbon nanotubes are used as novel tools to non-invasively track equilibrium and non-equilibrium fluctuations in such biopolymer networks. Here we analytically calculate shape fluctuations of semiflexible probe filaments in a viscoelastic environment, driven out of equilibrium by motor activity. Transverse bending fluctuations of the probe filaments can be decomposed into dynamic normal modes. We find that these modes no longer evolve independently under non-equilibrium driving. This effective mode coupling results in non-zero circulatory currents in a conformational phase space, reflecting a violation of detailed balance. We present predictions for the characteristic frequencies associated with these currents and investigate how the temporal signatures of motor activity determine mode correlations, which we find to be consistent with recent experiments on microtubules embedded in cytoskeletal networks.
The evolution of cooperation in social dilemmas in structured populations has been studied extensively in recent years. Whereas many theoretical studies have found that a heterogeneous network of contacts favors cooperation, the impact of spatial effects in scale-free networks is still not well understood. In addition to being heterogeneous, real contact networks exhibit a high mean local clustering coefficient, which implies the existence of an underlying metric space. Here, we show that evolutionary dynamics in scale-free networks self-organize into spatial patterns in the underlying metric space. The resulting metric clusters of cooperators are able to survive in social dilemmas as their spatial organization shields them from surrounding defectors, similar to spatial selection in Euclidean space. We show that under certain conditions these metric clusters are more efficient than the most connected nodes at sustaining cooperation and that heterogeneity does not always favor--but can even hinder--cooperation in social dilemmas. Our findings provide a new perspective to understand the emergence of cooperation in evolutionary games in realistic structured populations.
How cells move through the three-dimensional extracellular matrix (ECM) is of increasing interest in attempts to understand important biological processes such as cancer metastasis. Just as in motion on flat surfaces, it is expected that experimental measurements of cell-generated forces will provide valuable information for uncovering the mechanisms of cell migration. However, the recovery of forces in fibrous biopolymer networks may suffer from large errors. Here, within the framework of lattice-based models, we explore possible issues in force recovery by solving the inverse problem: how can one determine the forces cells exert to their surroundings from the deformation of the ECM? Our results indicate that irregular cell traction patterns, the uncertainty of local fiber stiffness, the non-affine nature of ECM deformations and inadequate knowledge of network topology will all prevent the precise force determination. At the end, we discuss possible ways of overcoming these difficulties.