It is unsatisfactory that regarding the problem of entangled macromolecules driven out of equilibrium, experimentally based understanding is usually inferred from the ensemble average of polydisperse samples. Here, confronting with single-molecule imaging this common but poorly understood situation, over a wide range of shear rate we use single-molecule fluorescence imaging to track alignment and stretching of entangled aqueous filamentous actin filaments in a homebuilt rheo-microscope. With increasing shear rate, tube “softening” is followed by “hardening.” Physically, this means that dynamical localization first weakens from molecular alignment, then strengthens from filament stretching, even for semiflexible biopolymers shorter than their persistence length.

The rheology of biological tissue plays an important role in many processes, from organ formation to cancer invasion. Here, we use a multiphase field model of motile cells to simulate active microrheology within a tissue monolayer. When unperturbed, the tissue exhibits a transition between a solidlike state and a fluidlike state tuned by cell motility and deformability—the ratio of the energetic costs of steric cell-cell repulsion and cell-edge tension. When perturbed, solid tissues exhibit local yield-stress behavior, with a threshold force for the onset of motion of a probe particle that vanishes upon approaching the solid-to-liquid transition. This onset of motion is qualitatively different in the low and high deformability regimes. At high deformability, the tissue is amorphous when solid, it responds compliantly to deformations, and the probe transition to motion is smooth. At low deformability, the monolayer is more ordered translationally and stiffer, and the onset of motion appears discontinuous. Our results suggest that cellular or nanoparticle transport in different types of tissues can be fundamentally different and point to ways in which it can be controlled.

The phenomenon that a system at a hot temperature cools faster than at a warm temperature, referred to as the Mpemba effect, has recently been realized for trapped colloids. Here, we investigate the cooling and heating process of a self-propelled active colloid using numerical simulations and theoretical calculations with a model that can be directly tested in experiments. Upon cooling, activity induces a Mpemba effect and the active particle transiently escapes an effective temperature description. At the end of the cooling process the notion of temperature is recovered and the system can exhibit even smaller temperatures than its final temperature, a surprising phenomenon which we refer to as activity-induced overcooling.

Here we show that encapsulating active Janus particles within a drop renders it more resistant to deformation. This drop is deformed under the action of an extensional flow. Such deformation is primarily resisted by the drop interfacial tension. When the particles are active under the action of laser illumination, the deformation decreases signaling an increase in effective tension or Laplace pressure. This increase is attributed to the activity of the particles. Our results using numerous drop sizes, particle number densities, and active velocities show that the obtained increase agrees surprisingly well, over an extended range, with a standard expression for the pressure engendered by an ensemble of active particles, proposed years ago but not tested yet in three dimensions.

Biological materials, such as the actin cytoskeleton, exhibit remarkable structural adaptability to various external stimuli by consuming different amounts of energy. In this Letter, we use methods from large deviation theory to identify a thermodynamic control principle for structural transitions in a model cytoskeletal network. Specifically, we demonstrate that biasing the dynamics with respect to the work done by nonequilibrium components effectively renormalizes the interaction strength between such components, which can eventually result in a morphological transition. Our work demonstrates how a thermodynamic quantity can be used to renormalize effective interactions, which in turn can tune structure in a predictable manner, suggesting a thermodynamic principle for the control of cytoskeletal structure and dynamics.

Biomolecular self-assembly spatially segregates proteins with a limited number of binding sites (valence) into condensates that coexist with a dilute phase. We develop a many-body lattice model for a three-component system of proteins with fixed valence in a solvent. We compare the predictions of the model to experimental phase diagrams that we measure in vivo, which allows us to vary specifically a binding site’s affinity and valency. We find that the extent of phase separation varies exponentially with affinity and increases with valency. Valency alone determines the symmetry of the phase diagram.

Semiflexible polymer glasses (SPGs), including those formed by the recently synthesized semiflexible conjugated polymers, are expected to be brittle because classical formulas for their craze extension ratio ${\lambda }_{\text{craze}}$ and fracture stretch ${\lambda }_{\mathrm{frac}}$ predict that systems with $N_e=C_{\infty }$ have ${\lambda }_{\text{craze}}={\lambda }_{\mathrm{frac}}=1$ and hence cannot be deformed to large strains. Using molecular dynamics simulations, we show that in fact such glasses can form stable crazes with ${\lambda }_{\text{craze}}\simeq N_e^{1/4}\simeq C_{\infty }^{1/4}$, and that they fracture at ${\lambda }_{\mathrm{frac}}=(3N_e^{1/2}-2{)}^{1/2}\simeq (3C_{\infty }^{1/2}-2{)}^{1/2}$. We argue that the classical formulas for ${\lambda }_{\text{craze}}$ and ${\lambda }_{\mathrm{frac}}$ fail to describe SPGs’ mechanical response because they do not account for Kuhn segments’ ability to stretch during deformation.

Fractures are a critical process in how materials wear, weaken, and fail, whose unpredictable behavior can have dire consequences. While the behavior of smooth cracks in ideal materials is well understood, it is assumed that for real, heterogeneous systems, fracture propagation is complex, generating rough fracture surfaces that are highly sensitive to specific details of the medium. Here we show how fracture roughness and material heterogeneity are inextricably connected via a simple framework. Studying hydraulic fractures in brittle hydrogels that have been supplemented with microbeads or glycerol to create controlled material heterogeneity, we show that the morphology of the crack surface depends solely on one parameter: the probability to perturb the front above a critical size to produce a steplike instability. This probability scales linearly with the number density, and with heterogeneity size to the $5/2$ power. The ensuing behavior is universal and is captured by the 1D ballistic propagation and annihilation of steps along the singular fracture front.

Growing axons are one-dimensional active structures that are important for wiring the brain and repairing nerves. However, the biophysical mechanisms underlying the complex kinetics of growing axons remain elusive. Here, we develop a theoretical framework to recapitulate force-regulated states and their transitions in growing axons. We demonstrate a unique negative feedback mechanism that defines four distinct kinetic states in a growing axon, whose transitional boundaries depend on the interplay between cytoskeletal dynamics and axon-substrate adhesion. A phase diagram for axonal growth is formulated based on two dimensionless numbers.

Molecular motors work collectively to transport cargo within cells, with anywhere from one to several hundred motors towing a single cargo. For a broad class of collective-transport systems, we use tools from stochastic thermodynamics to derive a new lower bound for the entropy production rate which is tighter than the second law. This implies new bounds on the velocity, efficiency, and precision of general transport systems and a set of analytic Pareto frontiers for identical motors. In a specific model, we identify conditions for saturation of these Pareto frontiers.

In the presence of long-range dispersal, epidemics spread in spatially disconnected regions known as clusters. Here, we characterize exactly their statistical properties in a solvable model, in both the supercritical (outbreak) and critical regimes. We identify two diverging length scales, corresponding to the bulk and the outskirt of the epidemic. We reveal a nontrivial critical exponent that governs the cluster number and the distribution of their sizes and of the distances between them. We also discuss applications to depinning avalanches with long-range elasticity.

Drug persistence is a phenomenon by which a small percentage of cancer cells survive the presentation of targeted therapy by transitioning to a quiescent state. Eventually some of these persister cells can transition back to an active growing state and give rise to resistant tumors. Here we introduce a quantitative genetics approach to drug-exposed populations of cancer cells in order to interpret recent experimental data regarding inheritance of persister probability. Our results indicate that alternating periods of drug treatment and drug removal may not be an effective strategy for eliminating persisters.

While stretching of a polymer along a flat surface is hardly different from the classical Pincus problem of pulling chain ends in free space, the role of curved geometry in conformational statistics of the stretched chain is an exciting open question. We use scaling analysis and computer simulations to examine stretching of a fractal polymer chain around a disc in 2D (or a cylinder in 3D) of radius $R$. We reveal that the typical excursions of the polymer away from the surface and curvature-induced correlation length scale as $\mathrm{\Delta }\sim R^{\beta }$ and $S^{*}\sim R^{1/z}$, respectively, with the Kardar-Parisi-Zhang (KPZ) growth $\beta =1/3$ and dynamic exponents $z=3/2$. Although probability distribution of excursions does not belong to KPZ universality class, the KPZ scaling is independent of the fractal dimension of the polymer and, thus, is universal across classical polymer models, e.g., SAW, randomly branching polymers, crumpled unknotted rings. Additionally, our Letter establishes a mapping between stretched polymers in curved geometry and the Balagurov-Vaks model of random walks among traps.

We determine the kinetic phase diagram for nucleation and growth of crystal phases in a suspension of charged colloids. Exploiting the seeding approach in extensive simulations, we calculate nucleation barrier heights for face-centered cubic (fcc) and body-centered cubic (bcc) phases for varying screening lengths and supersaturations. We determine for the entire metastable fluid region the crystal polymorph with the lowest nucleation barrier, and find a regime close to the triple point where metastable bcc can form due to a lower nucleation barrier, even though fcc is the stable phase. For higher supersaturation, we find that the difference in barrier heights decreases and we observe a mix of hexagonal close-packed, fcc, and bcc structures in the growth of crystalline seeds as well as in spontaneously formed crystals. Our kinetic phase diagram rationalizes the different crystallization mechanisms observed in previous work.

Inspired by recent experiments that highlight the role of nematic defects in the morphogenesis of epithelial tissues, we develop a minimal framework to study the dynamics of an active curved surface driven by its nematic texture. Allowing the surface to evolve via relaxational dynamics leads to a theory linking nematic defect dynamics, cellular division rates, and Gaussian curvature. Regions of large positive (negative) curvature and positive (negative) growth are colocalized with the presence of positive (negative) defects. In an ex-vivo setting of cultured murine neural progenitor cells, we show that our framework is consistent with the observed cell accumulation at positive defects and depletion at negative defects. In an in-vivo setting, we show that the defect configuration consisting of a bound $+1$ defect state, which is stabilized by activity, surrounded by two $-1/2$ defects can create a stationary ring configuration of tentacles, consistent with observations of a basal marine invertebrate Hydra.

Animal cells are active, contractile objects. While bioassays address the molecular characterization of cell contractility, the mechanical characterization of the active forces in cells remains challenging. Here by confronting theoretical analysis and experiments, we calculated both the resistive and the active components of the intracellular stresses that build up following cell adhesion. We obtained a linear relationship between the divergence of the passive stress and the traction forces, which we show is the consequence of the cell adhering and applying forces on the surface only through very localized adhesion points (whose size is inferior to our best resolution, of 400 nm). This entails that there are no measurable forces outside of these active point sources, and also that the passive stresses and active stresses inside cells are proportional.