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Martin Lenz

Publications and source records attributed to Martin Lenz.

36 records · Page 2Linked to original sources

Stress-dependent amplification of active forces in nonlinear elastic media

The production of mechanical stresses in living organisms largely relies on localized, force-generating active units embedded in filamentous matrices. Numerical simulations of discrete fiber networks with fixed boundaries have shown that buckling in the matrix dramatically amplifies the resulting active stresses. Here we extend this result to a bucklable continuum elastic medium subjected to an arbitrary external stress, and derive analytical expressions for the active, nonlinear constitutive relations characterizing the full active medium. Inserting these relations into popular "active gel" descriptions of living tissues and the cytoskeleton will enable investigations into nonlinear regimes previously inaccessible due to the phenomenological nature of these theories.

physics.bio-ph↗

Homogenization in magnetic-shape-memory polymer composites

Magnetic-shape-memory materials (e.g. specific NiMnGa alloys) react with a large change of shape to the presence of an external magnetic field. As an alternative for the difficult to manifacture single crystal of these alloys we study composite materials in which small magnetic-shape-memory particles are embedded in a polymer matrix. The macroscopic properties of the composite depend strongly on the geometry of the microstructure and on the characteristics of the particles and the polymer. We present a variational model based on micromagnetism and elasticity, and derive via homogenization an effective macroscopic model under the assumption that the microstructure is periodic. We then study numerically the resulting cell problem, and discuss the effect of the microstructure on the macroscopic material behavior. Our results may be used to optimize the shape of the particles and the microstructure.

math.AP↗

Stability from activity

Suspensions of actively driven anisotropic objects exhibit distinctively nonequilibrium behaviors, and current theories predict that they are incapable of sustaining orientational order at high activity. By contrast, here we show that nematic suspensions on a substrate can display order at arbitrarily high activity due to a previously unreported, potentially stabilizing active force. The resulting nonequilibrium ordered phase displays robust giant number fluctuations that cannot be suppressed even by an incompressible solvent. Our results apply to virtually all experimental assays used to investigate the active nematic ordering of self-propelled colloids, bacterial suspensions and the cytoskeleton, and have testable implications in interpreting their nonequilibrium behaviors

cond-mat.soft↗

Extensile actomyosin?

Living cells move thanks to assemblies of actin filaments and myosin motors that range from very organized striated muscle tissue to disordered intracellular bundles. The mechanisms powering these disordered structures are debated, and all models studied so far predict that they are contractile. We reexamine this prediction through a theoretical treatment of the interplay of three well-characterized internal dynamical processes in actomyosin bundles: actin treadmilling, the attachement-detachment dynamics of myosin and that of crosslinking proteins. We show that these processes enable an extensive control of the bundle's active mechanics, including reversals of the filaments' apparent velocities and the possibility of generating extension instead of contraction. These effects offer a new perspective on well-studied in vivo systems, as well as a robust criterion to experimentally elucidate the underpinnings of actomyosin activity.

physics.bio-ph↗

Cell contraction induces long-ranged stress stiffening in the extracellular matrix

Animal cells in tissues are supported by biopolymer matrices, which typically exhibit highly nonlinear mechanical properties. While the linear elasticity of the matrix can significantly impact cell mechanics and functionality, it remains largely unknown how cells, in turn, affect the nonlinear mechanics of their surrounding matrix. Here we show that living contractile cells are able to generate a massive stiffness gradient in three distinct 3D extracellular matrix model systems: collagen, fibrin, and Matrigel. We decipher this remarkable behavior by introducing Nonlinear Stress Inference Microscopy (NSIM), a novel technique to infer stress fields in a 3D matrix from nonlinear microrheology measurement with optical tweezers. Using NSIM and simulations, we reveal a long-ranged propagation of cell-generated stresses resulting from local filament buckling. This slow decay of stress gives rise to the large spatial extent of the observed cell-induced matrix stiffness gradient, which could form a mechanism for mechanical communication between cells.

physics.bio-ph↗

Geometrical frustration yields fiber formation in self-assembly

Controlling the self-assembly of supramolecular structures is vital for living cells, and a central challenge for engineering at the nano- and microscales. Nevertheless, even particles without optimized shapes can robustly form well-defined morphologies. This is the case in numerous medical conditions where normally soluble proteins aggregate into fibers. Beyond the diversity of molecular mechanisms involved, we propose that fibers generically arise from the aggregation of irregular particles with short-range interactions. Using a minimal model of ill-fitting, sticky particles, we demonstrate robust fiber formation for a variety of particle shapes and aggregation conditions. Geometrical frustration plays a crucial role in this process, and accounts for the range of parameters in which fibers form as well as for their metastable character.

cond-mat.soft↗

A posteriori modeling error estimates in the optimization of two-scale elastic composite materials

The a posteriori analysis of the discretization error and the modeling error is studied for a compliance cost functional in the context of the optimization of composite elastic materials and a two-scale linearized elasticity model. A mechanically simple, parametrized microscopic supporting structure is chosen and the parameters describing the structure are determined minimizing the compliance objective. An a posteriori error estimate is derived which includes the modeling error caused by the replacement of a nested laminate microstructure by this considerably simpler microstructure. Indeed, nested laminates are known to realize the minimal compliance and provide a benchmark for the quality of the microstructures. To estimate the local difference in the compliance functional the dual weighted residual approach is used. Different numerical experiments show that the resulting adaptive scheme leads to simple parametrized microscopic supporting structures that can compete with the optimal nested laminate construction. The derived a posteriori error indicators allow to verify that the suggested simplified microstructures achieve the optimal value of the compliance up to a few percent. Furthermore, it is shown how discretization error and modeling error can be balanced by choosing an optimal level of grid refinement. Our two scale results with a single scale microstructure can provide guidance towards the design of a producible macroscopic fine scale pattern.

math.NA↗

The dynamics of filament assembly define cytoskeletal network morphology

The actin cytoskeleton is a key component in the machinery of eukaryotic cells, and it selfassembles out of equilibrium into a wide variety of biologically crucial structures. While the molecular mechanisms involved are well characterized, the physical principles governing the spatial arrangement of actin filaments are not understood. Here we propose that the dynamics of actin network assembly from growing filaments results from a competition between diffusion, bundling, and steric hindrance, and is responsible for the range of observed morphologies. Our model and simulations thus predict an abrupt dynamical transition between homogeneous and strongly bundled networks as a function of the actin polymerization rate. This suggests that cells may effect dramatic changes to their internal architecture through minute modifications of their nonequilibrium dynamics. Our results are consistent with available experimental data.

cond-mat.soft↗

Fiber networks amplify active stress

Large-scale force generation is essential for biological functions such as cell motility, embryonic development, and muscle contraction. In these processes, forces generated at the molecular level by motor proteins are transmitted by disordered fiber networks, resulting in large-scale active stresses. While these fiber networks are well characterized macroscopically, this stress generation by microscopic active units is not well understood. Here we theoretically study force transmission in these networks, and find that local active forces are rectified towards isotropic contraction and strongly amplified as fibers collectively buckle in the vicinity of the active units. This stress amplification is reinforced by the networks' disordered nature, but saturates for high densities of active units. Our predictions are quantitatively consistent with experiments on reconstituted tissues and actomyosin networks, and shed light on the role of the network microstructure in shaping active stresses in cells and tissue.

cond-mat.soft↗

A Reaction-Diffusion Model of the Cadherin-Catenin System: A Possible Mechanism for Contact Inhibition and Implications for Tumorigenesis

Contact inhibition is the process by which cells switch from a motile growing state to a passive and stabilized state upon touching their neighbors. When two cells touch, an adhesion link is created between them by means of transmembrane E-cadherin proteins. Simultaneously, their actin filaments stop polymerizing in the direction perpendicular to the membrane and reorganize to create an apical belt that colocalizes with the adhesion links. Here, we propose a detailed quantitative model of the role of the cytoplasmic $β$-catenin and $α$-catenin proteins in this process, treated as a reaction-diffusion system. Upon cell-cell contact, the concentration in $α$-catenin dimers increases, inhibiting actin branching and thereby reducing cellular motility and expansion pressure. This model provides a mechanism for contact inhibition that could explain previously unrelated experimental findings on the role played by E-cadherin, $β$-catenin and $α$-catenin in the cellular phenotype and in tumorigenesis. In particular, we address the effect of a knockout of the adenomatous polyposis coli tumor suppressor gene. Potential direct tests of our model are discussed.

physics.bio-ph↗

Hysteresis in Magnetic Shape Memory Composites: Modeling and Simulation

Magnetic shape memory alloys are characterized by the coupling between a structural phase transition and magnetic one. This permits to control the shape change via an external magnetic field, at least in single crystals. Composite materials with single-crystalline particles embedded in a softer matrix have been proposed as a way to overcome the blocking of the transformation at grain boundaries. We investigate hysteresis phenomena for small NiMnGa single crystals embedded in a polymer matrix for slowly varying magnetic fields. The evolution of the microstructure is studied within the rate-independent variational framework proposed by Mielke and Theil (1999). The underlying variational model incorporates linearized elasticity, micromagnetism, stray field and a dissipation term proportional to the volume swept by the phase boundary. The time discretization is based on an incremental minimization of the sum of energy and dissipation. A backtracking approach is employed to approximately ensure the global minimality condition. We illustrate and discuss the influence of the particle geometry (volume fraction, shape, arrangement) and the polymer elastic parameters on the observed hysteresis and compare with recent experimental results.

math.NA↗

Connecting local active forces to macroscopic stress in elastic media

In contrast with ordinary materials, living matter drives its own motion by generating active, out-of-equilibrium internal stresses. These stresses typically originate from localized active elements embedded in an elastic medium, such as molecular motors inside the cell or contractile cells in a tissue. While many large-scale phenomenological theories of such active media have been developed, a systematic understanding of the emergence of stress from the local force-generating elements is lacking. In this paper, we present a rigorous theoretical framework to study this relationship. We show that the medium's macroscopic active stress tensor is equal to the active elements' force dipole tensor per unit volume in both continuum and discrete linear homogeneous media of arbitrary geometries. This relationship is conserved on average in the presence of disorder, but can be violated in nonlinear elastic media. Such effects can lead to either a reinforcement or an attenuation of the active stresses, giving us a glimpse of the ways in which nature might harness microscopic forces to create active materials.

cond-mat.soft↗

Geometrical origins of contractility in disordered actomyosin networks

Movement within eukaryotic cells largely originates from localized forces exerted by myosin motors on scaffolds of actin filaments. Although individual motors locally exert both contractile and extensile forces, large actomyosin structures at the cellular scale are overwhelmingly contractile, suggesting that the scaffold serves to favor contraction over extension. While this mechanism is well understood in highly organized striated muscle, its origin in disordered networks such as the cell cortex is unknown. Here we develop a mathematical model of the actin scaffold's local two- or three-dimensional mechanics and identify four competing contraction mechanisms. We predict that one mechanism dominates, whereby local deformations of the actin break the balance between contraction and extension. In this mechanism, contractile forces result mostly from motors plucking the filaments transversely rather than buckling them longitudinally. These findings sheds light on recent $\textit{in vitro}$ experiments, and provides a new geometrical understanding of contractility in the myriad of disordered actomyosin systems found $\textit{in vivo}$.

physics.bio-ph↗

Dynamical tunnelling with ultracold atoms in magnetic microtraps

The study of dynamical tunnelling in a periodically driven anharmonic potential probes the quantum-classical transition via the experimental control of the effective Planck's constant for the system. In this paper we consider the prospects for observing dynamical tunnelling with ultracold atoms in magnetic microtraps on atom chips. We outline the driven anharmonic potentials that are possible using standard magnetic traps, and find the Floquet spectrum for one of these as a function of the potential strength, modulation, and effective Planck's constant. We develop an integrable approximation to the non-integrable Hamiltonian and find that it can explain the behaviour of the tunnelling rate as a function of the effective Planck's constant in the regular region of parameter space. In the chaotic region we compare our results with the predictions of models that describe chaos-assisted tunnelling. Finally we examine the practicality of performing these experiments in the laboratory with Bose-Einstein condensates.

cond-mat.quant-gas↗

Requirements for contractility in disordered cytoskeletal bundles

Actomyosin contractility is essential for biological force generation, and is well understood in highly organized structures such as striated muscle. Additionally, actomyosin bundles devoid of this organization are known to contract both in vivo and in vitro, which cannot be described by standard muscle models. To narrow down the search for possible contraction mechanisms in these systems, we investigate their microscopic symmetries. We show that contractile behavior requires non-identical motors that generate large enough forces to probe the nonlinear elastic behavior of F-actin. This suggests a role for filament buckling in the contraction of these bundles, consistent with recent experimental results on reconstituted actomyosin bundles.

physics.bio-ph↗

Contractile units in disordered actomyosin bundles arise from F-actin buckling

Bundles of filaments and motors are central to contractility in cells. The classic example is striated muscle, where actomyosin contractility is mediated by highly organized sarcomeres which act as fundamental contractile units. However, many contractile bundles in vivo and in vitro lack sarcomeric organization. Here we propose a model for how contractility can arise in actomyosin bundles without sarcomeric organization and validate its predictions with experiments on a reconstituted system. In the model, internal stresses in frustrated arrangements of motors with diverse velocities cause filaments to buckle, leading to overall shortening. We describe the onset of buckling in the presence of stochastic actin-myosin detachment and predict that buckling-induced contraction occurs in an intermediate range of motor densities. We then calculate the size of the "contractile units" associated with this process. Consistent with these results, our reconstituted actomyosin bundles contract at relatively high motor density, and we observe buckling at the predicted length scale.

physics.bio-ph↗

Membrane buckling induced by curved filaments

We present a novel buckling instability relevant to membrane budding in eukaryotic cells. In this mechanism, curved filaments bind to a lipid bilayer without changing its intrinsic curvature. As more and more filaments adsorb, newly added ones are more and more strained, which destabilizes the flat membrane. We perform a linear stability analysis of filament-dressed membranes and find that the buckling threshold is within reasonable in vivo parameter values. We account for the formation of long tubes previously observed in cells and in purified systems. We study strongly deformed dressed membranes and their bifurcation diagram numerically. Our mechanism could be validated by a simple experiment.

physics.bio-ph↗

Mechanochemical action of the dynamin protein

Dynamin is a ubiquitous GTPase that tubulates lipid bilayers and is implicated in many membrane severing processes in eukaryotic cells. Setting the grounds for a better understanding of this biological function, we develop a generalized hydrodynamics description of the conformational change of large dynamin-membrane tubes taking into account GTP consumption as a free energy source. On observable time scales, dissipation is dominated by an effective dynamin/membrane friction and the deformation field of the tube has a simple diffusive behavior, which could be tested experimentally. A more involved, semi-microscopic model yields complete predictions for the dynamics of the tube and possibly accounts for contradictory experimental results concerning its change of conformation as well as for plectonemic supercoiling.

cond-mat.soft↗