Kristian Thijssen

Dense active materials must continuously relieve internal mechanical stress to remain structurally stable as they are driven far from equilibrium. In epithelial tissues, this relief occurs through cell division, where, according to Hertwig’s century-old rule, cells divide along their long axis. We show that as epithelia densify, this geometric rule is superseded by a mechanical one: cells divide along the principal axis of anisotropic stress, independently of the isotropic stress state. Using direct force measurements and stress inference, we demonstrate that stress orientation governs division across mechanically distinct systems, from fluid-like to jammed monolayers and structurally heterogeneous organoids, remaining predictive where cell shape fails. This stress-oriented remodeling is reciprocally coupled to the material’s mechanical state: anisotropic stress accelerates cell-cycle progression, while division locally dissipates it, closing a negative feedback loop. This “principal-stress rule” provides a general mechanical framework linking internal stress, structural remodeling and homeostasis in living materials.

Dense active materials, from cellular tissues to jammed and glassy systems, must continuously relieve internal mechanical stress to remain structurally stable as they are driven far from equilibrium. In epithelial tissues, this relief occurs through cell division, yet what sets the geometry of this structural remodeling event has, for over a century, been attributed to a purely geometric principle: Hertwig’s rule, whereby cells divide along their long axis. We show that as epithelial tissues densify and cell shape anisotropy collapses, this geometric rule is superseded by a mechanical one in which dense epithelia relieve anisotropic stress by cells dividing along their principal axis, independent of the tissue’s isotropic stress state. Using direct force measurement and stress inference, we show that stress orientation, rather than cell shape, governs the axis of cell division across mechanically distinct systems, from fluid-like to jammed monolayers and structurally heterogeneous organoids, remaining predictive precisely where the classical geometric rule fails. This stress-oriented remodeling is reciprocally coupled to the material’s mechanical state: anisotropic stress accelerates the underlying remodeling rate, while each remodeling event locally dissipates the stress that triggered it, closing a negative feedback loop. This “principal-stress rule” recasts epithelial cell division as a stress-relief mechanism intrinsic to dense active matter, providing a general mechanical framework linking internal stress, structural remodeling, and homeostasis in living materials.

We investigate how coupling to fluid flow influences defect-mediated transitions in two-dimensional passive and active nematic fluids using fluctuating nematohydrodynamic simulations. The system is driven by tuning the fluctuation strength, with increasing (decreasing) fluctuations defining the forward (backward) protocol through the defect creation temperature threshold where defects spontaneously nucleate. In the absence of flow coupling, the transition follows the Berezinskii–Kosterlitz–Thouless (BKT) scenario, governed by reversible binding and unbinding of ± 1 / 2 defect pairs. When hydrodynamics is included, the outcome is controlled by the flow-alignment parameter. For non-aligning nematics ( λ = 0), the transition remains consistent with BKT. By contrast, for strain-rate–coupled nematics ( λ ≠ 0), bend–splay walls emerge, lowering the defect nucleation threshold and preventing sustained recombination: once created, defects remain unbound across the full range of fluctuation strengths in both forward and backward protocols. In active nematics, self-generated flows produce the same effect, with defects remaining unbound irrespective of alignment. These findings demonstrate that coupling to flow, whether through strain-rate alignment or activity, fundamentally alters defect-mediated phase transitions and suggest that the canonical BKT transition emerges only in the absence of flow coupling.

Bacterial competition shapes community architecture, yet a universally conserved determinant remains elusive. We show that cell aspect ratio –a simple morphological feature– confers a competitive advantage. Using growth-based range expansion experiments, we show that longer bacteria conquer the expanding front, even when initially in minority. Using an agent-based model of dividing bacteria, to isolate the effect of aspect ratio, we reveal that the takeover mechanism is collective alignment: groups of locally aligned bacteria form “nematic arms” bridging the central region of the colony to the expanding front. Once at the front, bacteria align parallel to it and block shorter bacteria from access to nutrients and space. We confirm this observation with single-cell experiments and further generalise our findings by introducing a generic continuum model of alignment-dominated competition, explaining both experimental and cell-based model observations. Moreover, we extend our predictions to spherical range expansions and confirm the competitive advantage, even though the effect is less pronounced than in surface-attached colonies. Our results uncover a simple, yet hitherto overlooked, mechanical mechanism determining the outcome of bacterial competition, which is potentially ubiquitous among various bacteria. Current advances in genetic engineering enable aspect ratio tuning as a mechanism with broad implications for biofilm control.

Understanding the mechanical properties of active suspensions is crucial for their potential applications in materials engineering. Among active phenomena with no analog in equilibrium systems, motility-induced phase separation (MIPS) in active colloidal suspensions is one of the most extensively studied. However, the mechanical properties of MIPS remain poorly understood. This Letter investigates the rheology of a suspension of active colloidal particles under constant and oscillatory shear. Systems consisting of pseudohard active Brownian particles exhibiting coexistence of dense and dilute phases behave as a viscoelastic Maxwell-like fluid at low and high frequencies, displaying exclusively shear thinning across a wide range of densities and activities. Remarkably, the crossover frequency between the storage and loss moduli is nonmonotonic, increasing with activity before the MIPS transition but decreasing with activity after the transition, in contrast to a passive analog system of attractive particles in liquid-gas phase coexistence, revealing the subtleties of how active forces and intrinsically out-of-equilibrium phases affect the mechanical properties.

Many physiological processes, such as the shear flow alignment of endothelial cells in the vasculature, depend on the transition of cell layers between disordered and ordered phases. Here we demonstrate that such a transition is driven by the non-monotonic evolution of nematic topological defects in a layer of endothelial cells and the emergence of string excitations that bind the defects together. This suggests the existence of an intermediate phase of ordering kinetics in biological matter. We use time-resolved large-scale imaging and physical modelling to analyse the non-monotonic decrease in the number of defect pairs. The interaction of the intrinsic cell layer activity and the alignment field determines the occurrence of defect domains, which defines the nature of the transition. Defect pair annihilation is mediated by string excitations spanning multicellular scales within the cell layer. Our results, therefore, suggest a mechanism by which intermediate ordering and string excitation might contribute to regulating morphogenetic movements and tissue remodelling in vivo.

Colloidal gels are prime examples of functional materials exhibiting disordered, amorphous, yet metastable forms. They maintain stability through short-range attractive forces and their material properties are tunable by external forces. Combining persistent homology analyses and simulations of three-dimensional colloidal gels doped with active particles, we reveal novel dynamically evolving structures of colloidal gels. Specifically, we show that the local injection of energy by active dopants can lead to highly porous, yet compact gel structures that can significantly affect the transport of active particles within the modified colloidal gel. We further show how passive interfaces play a topologically significant role in interacting with active particles in 3D. The results open the door to an unexplored prospect of forming a wide variety of compact but highly heterogeneous and percolated porous media through active doping of 3D passive matter, with diverse implications in designing new functional materials for active ground remediation.

While bacterial swarms can exhibit active turbulence in vacant spaces, they naturally inhabit crowded environments. We numerically show that driving disorderly active fluids through porous media enhances Darcy’s law. While purely active flows average to zero flux, hybrid active/driven flows display greater drift than purely pressure-driven flows. This enhancement is nonmonotonic with activity, leading to an optimal activity to maximize flow rate. We incorporate the active contribution into an active Darcy’s law, which may serve to help understand anomalous transport of swarming in porous media. Published by the American Physical Society 2024

Bacteria’s competition for nutrients and territory drives biofilm evolution (1 –4). The factors determining the outcome of competition among diverse bacterial species have a broad impact on a wide range of pathological (5), environmental (6), and microbiome interactions (7). While motility-related traits (8 – 11) and specific molecular mechanisms (12 , 13) have been identified as potential winning attributes in bacteria, a shared and universally conserved feature determining competition remains elusive. Here, we demonstrate that a simple morphological feature of individual bacteria, cell aspect ratio, provides a winning trait for the population. Using range expansion experiments (14), we show that relatively longer bacteria robustly conquer the expanding front, even when initially in minority. Using an agent based model of dividing bacteria, we reveal that the takeover mechanism is their emergent collective alignment: groups of locally aligned bacteria form "nematic arms" bridging the central region of the colony to the expanding front. Once at the front, bacteria align parallel to it and block the access of shorter bacteria to nutrients and space. We confirm this observation with single-cell experiments and further generalise our findings by introducing a generic continuum model of alignment-dominated competition, explaining both experimental and cell-based model observations. Moreover, we extend our predictions to spherical range expansions (15) and confirm the competitive advantage of being longer, even though the effect is less pronounced than in surface-attached colonies. Our results uncover a simple, yet hitherto overlooked, mechanical mechanism determining the outcome of bacterial competition, which is potentially ubiquitous among various bacteria. With the current advances in genetic engineering, varying aspect ratios can work as a simple tunable mechanism for the on-demand setting of the outcome of bacterial competitions with widespread implications for biofilm control.

Bacterial competition shapes community architecture, yet a universally conserved determinant remains elusive. We show that cell aspect ratio –a simple morphological feature– confers a competitive advantage. Using growth-based range expansion experiments, we show that longer bacteria conquer the expanding front, even when initially in minority. Using an agent-based model of dividing bacteria, to isolate the effect of aspect ratio, we reveal that the takeover mechanism is collective alignment: groups of locally aligned bacteria form “nematic arms” bridging the central region of the colony to the expanding front. Once at the front, bacteria align parallel to it and block shorter bacteria from access to nutrients and space. We confirm this observation with single-cell experiments and further generalise our findings by introducing a generic continuum model of alignment-dominated competition, explaining both experimental and cell-based model observations. Moreover, we extend our predictions to spherical range expansions and confirm the competitive advantage, even though the effect is less pronounced than in surface-attached colonies. Our results uncover a simple, yet hitherto overlooked, mechanical mechanism determining the outcome of bacterial competition, which is potentially ubiquitous among various bacteria. Current advances in genetic engineering enable aspect ratio tuning as a mechanism with broad implications for biofilm control.