arXiv subjects

Jaume Casademunt

Publications and source records attributed to Jaume Casademunt.

At least 19 recordsLinked to original sources

arXiv2026

Bistability of cellular traction on strain-stiffening substrates

To migrate, cells exert traction forces on the extracellular matrix (ECM) -- a biopolymer network that often exhibits nonlinear strain-stiffening elasticity. Cellular tractions can therefore stiffen the ECM. At the same time, cells exert stronger tractions on stiffer ECM. Here, we show theoretically that this traction-stiffness feedback can produce traction bistability and hysteresis. As a result, increasing either the ECM's nonlinear elasticity or cellular contractility leads to a discontinuous transition from low to high tractions. This traction jump might trigger collective cell migration as the ECM stiffens, for example during development and tumor progression. Moreover, the bistable behavior might provide robustness to cellular traction forces when cells migrate through mechanically heterogeneous environments.

physics.bio-ph↗

arXiv2025

Dynamical arrest in active nematic turbulence

Active fluids display spontaneous turbulent-like flows known as active turbulence. Recent work revealed that these flows have universal features, independent of the material properties and of the presence of topological defects. However, the differences between defect-laden and defect-free active turbulence remain largely unexplored. Here, by means of large-scale numerical simulations, we show that defect-free active nematic turbulence can undergo dynamical arrest. This state is characterized by an emergent network of nematic domain walls that channels coherent streams and suppresses chaotic flows. As the system evolves, the branched wall network produces a large-scale pattern with tree-like topological properties. We find that flow alignment -- the tendency of nematics to reorient under shear -- enhances large-scale chaotic jets in contractile rodlike systems while promoting dynamical arrest in extensile systems. We further show that dynamical arrest persists regardless of whether defects are prohibited by construction or simply fail to form due to a high energy cost of defect cores. Taken together, our findings reveal a striking pattern-formation mechanism, with labyrinths emerging from active turbulence, and illuminate the rich transitional regime between defect-free and defect-laden dynamics. These behaviors call for the experimental realization of active nematics at vanishing or low defect densities, and underscore that, in extensile rodlike nematics, topological defects enable turbulence by preventing dynamical arrest.

cond-mat.soft↗

arXiv2025

Cell clusters sense their global shape to drive collective migration

The collective migration of epithelial groups of cells plays a central role in processes such as embryo development, wound healing, and cancer invasion. While finite cell clusters are known to collectively migrate in response to external gradients, the competing effect of possible endogenous cues is largely unknown.Here, we demonstrate that the polarization of peripheral cells that pull the cluster's edge outward is sufficient to induce and sustain the collective migration of confluent clusters. We use a general continuum model to show that the underlying shape-sensing mechanism is purely mechanical, relying on long-range hydrodynamic interactions and cell-cell alignment forces. As a proof-of-concept, we validate our findings with experiments on monolayer clusters from various cell lines, where we control initial shapes and sizes. The mechanism operates independently of external signals and will generally interfere with them. Specifically, we predict and observe experimentally that it can override collective durotaxis, reversing the direction of migration. Together, our results offer a physical framework for understanding how cell interactions govern the interplay between global shape and collective motion and afford engineering principles for optimal control and manipulation of cell cluster shape and motion.

physics.bio-ph↗

arXiv2024

Nonlinear spontaneous flow instability in active nematics

Active nematics exhibit spontaneous flows through a well-known linear instability of the uniformly-aligned quiescent state. Here we show that even a linearly stable uniform state can experience a nonlinear instability, resulting in a discontinuous transition to spontaneous flows. In this case, quiescent and flowing states may coexist. Through a weakly nonlinear analysis and a numerical study, we trace the bifurcation diagram of striped patterns and show that the underlying pitchfork bifurcation switches from supercritical (continuous) to subcritical (discontinuous) by varying the flow-alignment parameter. We predict that the discontinuous spontaneous flow transition occurs for a wide range of parameters, including systems of contractile flow-aligning rods. Our predictions are relevant to active nematic turbulence and can potentially be tested in experiments on either cell layers or active cytoskeletal suspensions.

cond-mat.soft↗

arXiv2021

Collective durotaxis of cohesive cell clusters on a stiffness gradient

Many types of motile cells perform durotaxis, namely, directed migration following gradients of substrate stiffness. Recent experiments have revealed that cell monolayers can migrate toward stiffer regions even when individual cells do not -- a phenomenon known as collective durotaxis. Here we address the spontaneous motion of finite cohesive cell monolayers on a stiffness gradient. We theoretically analyze a continuum active polar fluid model that has been tested in recent wetting assays of epithelial tissues, and includes two types of active forces (cell-substrate traction and cell-cell contractility). The competition between the two active forces determines whether a cell monolayer spreads or contracts. Here, we show that this model generically predicts collective durotaxis, and that it features a variety of dynamical regimes as a result of the interplay between the spreading state and the global propagation, including sequential contraction and spreading of the monolayer as it moves toward higher stiffness. We solve the model exactly in some relevant cases, which provides both physical insights into the mechanisms of tissue durotaxis and spreading as well as a variety of predictions that could guide the design of future experiments.

physics.bio-ph↗

arXiv2021

Active Turbulence

Active fluids exhibit spontaneous flows with complex spatiotemporal structure, which have been observed in bacterial suspensions, sperm cells, cytoskeletal suspensions, self-propelled colloids, and cell tissues. Despite occurring in the absence of inertia, chaotic active flows are reminiscent of inertial turbulence, and hence they are known as active turbulence. Here, we survey the field, providing a unified perspective over different classes of active turbulence. To this end, we divide our review in sections for systems with either polar or nematic order, and with or without momentum conservation (wet/dry). Comparing to inertial turbulence, we highlight the emergence of power-law scaling with either universal or non-universal exponents. We also contrast scenarios for the transition from steady to chaotic flows, and we discuss the absence of energy cascades. We link this feature to both the existence of intrinsic length scales and the self-organized nature of energy injection in active turbulence, which are fundamental differences with inertial turbulence. We close by outlining the emerging picture, remaining challenges, and future directions.

cond-mat.soft↗

arXiv2021

Scaling regimes of active turbulence with external dissipation

Active fluids exhibit complex turbulent-like flows at low Reynolds number. Recent work predicted that 2d active nematic turbulence follows universal scaling laws. However, experimentally testing these predictions is conditioned by the coupling to the 3d environment. Here, we measure the spectrum of the kinetic energy, $E(q)$, in an active nematic film in contact with a passive oil layer. At small and intermediate scales, we find the scaling regimes $E(q)\sim q^{-4}$ and $E(q)\sim q^{-1}$, respectively, in agreement with the theoretical prediction for 2d active nematics. At large scales, however, we find a new scaling $E(q)\sim q$, which emerges when the dissipation is dominated by the 3d oil layer. In addition, we derive an explicit expression for the spectrum that spans all length scales, thus explaining and connecting the different scaling regimes. This allows us to fit the data and extract the length scale that controls the crossover to the new large-scale regime, which we tune by varying the oil viscosity. Overall, our work experimentally demonstrates the emergence of universal scaling laws in active turbulence, and it establishes how the spectrum is affected by external dissipation.

cond-mat.soft↗

arXiv2020

Stochastic quorum percolation and noise focusing in neuronal networks

Recent experiments have shown that the spontaneous activity of young dissociated neuronal cultures can be described as a process of highly inhomogeneous nucleation and front propagation due to the localization of noise activity, i.e., noise focusing. However, the basic understanding of the mechanisms of noise build-up leading to the nucleation remain an open fundamental problem. Here we present a minimal dynamical model called stochastic quorum percolation that can account for the observed phenomena, while providing a robust theoretical framework. The model reproduces the first and second order phase--transitions of bursting dynamics and neuronal avalanches respectively, and captures the profound effect metric correlations in the network topology can have on the dynamics. The application of our results to other systems such as in the propagation of infectious diseases and of rumors is discussed.

q-bio.NC↗

arXiv2020

Universal scaling of active nematic turbulence

A landmark of turbulence is the emergence of universal scaling laws, such as Kolmogorov's $E(q)\sim q^{-5/3}$ scaling of the kinetic energy spectrum of inertial turbulence with the wave vector $q$. In recent years, active fluids have been shown to exhibit turbulent-like flows at low Reynolds number. However, the existence of universal scaling properties in these flows has remained unclear. To address this issue, here we propose a minimal defect-free hydrodynamic theory for two-dimensional active nematic fluids at vanishing Reynolds number. By means of large-scale simulations and analytical arguments, we show that the kinetic energy spectrum exhibits a universal scaling $E(q)\sim q^{-1}$ at long wavelengths. We find that the energy injection due to activity has a peak at a characteristic length scale, which is selected by a nonlinear mechanism. In contrast to inertial turbulence, energy is entirely dissipated at the scale where it is injected, thus precluding energy cascades. Nevertheless, the non-local character of the Stokes flow establishes long-ranged velocity correlations, which lead to the scaling behavior. We conclude that active nematic fluids define a distinct universality class of turbulence at low Reynolds number.

cond-mat.soft↗

arXiv2020

Role of Substrate Stiffness in Tissue Spreading: Wetting Transition and Tissue Durotaxis

Living tissues undergo wetting transitions: On a surface, they can either form a droplet-like cell aggregate or spread as a monolayer of migrating cells. Tissue wetting depends not only on the chemical but also on the mechanical properties of the substrate. Here, we study the role of substrate stiffness in tissue spreading, which we describe by means of an active polar fluid model. Taking into account that cells exert larger active traction forces on stiffer substrates, we predict a tissue wetting transition at a critical substrate stiffness that decreases with tissue size. On substrates with a stiffness gradient, we find that the tissue spreads faster on the stiffer side. Further, we show that the tissue can wet the substrate on the stiffer side while dewetting from the softer side. We also show that, by means of viscous forces transmitted across the tissue, the stiffer-side interface can transiently drag the softer-side interface towards increasing stiffness, against its spreading tendency. These two effects result in directed tissue migration up the stiffness gradient. This phenomenon -- tissue durotaxis -- can thus emerge both from dewetting at the soft side and from hydrodynamic interactions between the tissue interfaces. Overall, our work unveils mechanisms whereby substrate stiffness impacts the collective migration and the active wetting properties of living tissues, which are relevant in development, regeneration, and cancer.

physics.bio-ph↗

arXiv2019

Active Fingering Instability in Tissue Spreading

During the spreading of epithelial tissues, the advancing tissue front often develops fingerlike protrusions. Their resemblance to traditional viscous fingering patterns in driven fluids suggests that epithelial fingers could arise from an interfacial instability. However, the existence and physical mechanism of such a putative instability remain unclear. Here, based on an active polar fluid model for epithelial spreading, we analytically predict a generic instability of the tissue front. On the one hand, active cellular traction forces impose a velocity gradient that leads to an accelerated front, which is, thus, unstable to long-wavelength perturbations. On the other hand, contractile intercellular stresses typically dominate over surface tension in stabilizing short-wavelength perturbations. Finally, the finite range of hydrodynamic interactions in the tissue selects a wavelength for the fingering pattern, which is, thus, given by the smallest between the tissue size and the hydrodynamic screening length. Overall, we show that spreading epithelia experience an active fingering instability based on a simple kinematic mechanism. Moreover, our results underscore the crucial role of long-range hydrodynamic interactions in the dynamics of tissue morphology.

physics.bio-ph↗

arXiv2019

Active wetting of epithelial tissues

Development, regeneration and cancer involve drastic transitions in tissue morphology. In analogy with the behavior of inert fluids, some of these transitions have been interpreted as wetting transitions. The validity and scope of this analogy are unclear, however, because the active cellular forces that drive tissue wetting have been neither measured nor theoretically accounted for. Here we show that the transition between 2D epithelial monolayers and 3D spheroidal aggregates can be understood as an active wetting transition whose physics differs fundamentally from that of passive wetting phenomena. By combining an active polar fluid model with measurements of physical forces as a function of tissue size, contractility, cell-cell and cell-substrate adhesion, and substrate stiffness, we show that the wetting transition results from the competition between traction forces and contractile intercellular stresses. This competition defines a new intrinsic lengthscale that gives rise to a critical size for the wetting transition in tissues, a striking feature that has no counterpart in classical wetting. Finally, we show that active shape fluctuations are dynamically amplified during tissue dewetting. Overall, we conclude that tissue spreading constitutes a prominent example of active wetting --- a novel physical scenario that may explain morphological transitions during tissue morphogenesis and tumor progression.

physics.bio-ph↗

arXiv2017

Mixed-order phase transition in a colloidal crystal

Mixed-order phase transitions display a discontinuity in the order parameter like first-order transitions yet feature critical behavior like second-order transitions. Such transitions have been predicted for a broad range of equilibrium and nonequilibrium systems, but their experimental observation has remained elusive. Here, we analytically predict and experimentally realize a mixed-order equilibrium phase transition. Specifically, a discontinuous solid-solid transition in a two-dimensional crystal of paramagnetic colloidal particles is induced by a magnetic field $H$. At the transition field $H_{\text{s}}$, the energy landscape of the system becomes completely flat, which causes diverging fluctuations and correlation length $ξ\propto | H^2 - H_{\text{s}}^2|^{-1/2}$. Mean-field critical exponents are predicted, since the upper critical dimension of the transition is $d_{\text{u}}=2$. Our colloidal system provides an experimental test bed to probe the unconventional properties of mixed-order phase transitions.

cond-mat.stat-mech↗

arXiv2017

Nonlinear amplitude dynamics in flagellar beating

The physical basis of flagellar and ciliary beating is a major problem in biology which is still far from completely understood. The fundamental cytoskeleton structure of cilia and flagella is the axoneme, a cylindrical array of microtubule doublets connected by passive crosslinkers and dynein motor proteins. The complex interplay of these elements leads to the generation of self-organized bending waves. Although many mathematical models have been proposed to understand this process, few attempts have been made to assess the role of dyneins on the nonlinear nature of the axoneme. Here, we investigate the nonlinear dynamics of flagella by considering an axonemal sliding control mechanism for dynein activity. This approach unveils the nonlinear selection of the oscillation amplitudes, which are typically either missed or prescribed in mathematical models. The explicit set of nonlinear equations are derived and solved numerically. Our analysis reveals the spatiotemporal dynamics of dynein populations and flagellum shape for different regimes of motor activity, medium viscosity and flagellum elasticity. Unstable modes saturate via the coupling of dynein kinetics and flagellum shape without the need of invoking a nonlinear axonemal response. Hence, our work reveals a novel mechanism for the saturation of unstable modes in axonemal beating.

physics.bio-ph↗

arXiv2017

Fluidization and Active Thinning by Molecular Kinetics in Active Gels

We derive the constitutive equations of an active polar gel from a model for the dynamics of elastic molecules that link polar elements. Molecular binding kinetics induces the fluidization of the material, giving rise to Maxwell viscoelasticity and, provided that detailed balance is broken, to the generation of active stresses. We give explicit expressions for the transport coefficients of active gels in terms of molecular properties, including nonlinear contributions on the departure from equilibrium. In particular, when activity favors linker unbinding, we predict a decrease of viscosity with activity - active thinning - of kinetic origin, which could explain some experimental results on the cell cortex. By bridging the molecular and hydrodynamic scales, our results could help understand the interplay between molecular perturbations and the mechanics of cells and tissues.

physics.bio-ph↗

arXiv2016

Formation of metastable phases by spinodal decomposition

Metastable phases may be spontaneously formed from other metastable phases through nucleation. Here we demonstrate the spontaneous formation of a metastable phase from an unstable equilibrium by spinodal decomposition, which leads to a transient coexistence of stable and metastable phases. This phenomenon is generic within the recently introduced scenario of the landscape-inversion phase transitions, which we experimentally realize as a structural transition in a colloidal crystal. This transition exhibits a rich repertoire of new phase-ordering phenomena, including the coexistence of two equilibrium phases connected by two physically different interfaces. In addition, this scenario enables the control of sizes and lifetimes of metastable domains. Our findings open a new setting that broadens the fundamental understanding of phase-ordering kinetics, and yield new prospects of applications in materials science.

cond-mat.soft↗

arXiv2016

Bleb Nucleation through Membrane Peeling

We study the nucleation of blebs, i.e., protrusions arising from a local detachment of the membrane from the cortex of a cell. Based on a simple model of elastic linkers with force-dependent kinetics, we show that bleb nucleation is governed by membrane peeling. By this mechanism, the growth or shrinkage of a detached membrane patch is completely determined by the linker kinetics, regardless of the energetic cost of the detachment. We predict the critical nucleation radius for membrane peeling and the corresponding effective energy barrier. These may be typically smaller than those predicted by classical nucleation theory, implying a much faster nucleation. We also perform simulations of a continuum stochastic model of membrane-cortex adhesion to obtain the statistics of bleb nucleation times as a function of the stress on the membrane. The determinant role of membrane peeling changes our understanding of bleb nucleation and opens new directions in the study of blebs.

physics.bio-ph↗

arXiv2016

Model for probing membrane-cortex adhesion by micropipette aspiration and fluctuation spectroscopy

We propose a model for membrane-cortex adhesion which couples membrane deformations, hydrodynamics and kinetics of membrane-cortex ligands. In its simplest form, the model gives explicit predictions for the critical pressure for membrane detachment and for the value of adhesion energy. We show that these quantities exhibit a significant dependence on the active acto-myosin stresses. The model provides a simple framework to access quantitative information on cortical activity by means of micropipette experiments. We also extend the model to incorporate fluctuations and show that detailed information on the stability of membrane-cortex coupling can be obtained by a combination of micropipette aspiration and fluctuation spectroscopy measurements.

physics.bio-ph↗