arXiv subjects

Pierre A. Haas

Publications and source records attributed to Pierre A. Haas.

At least 19 recordsLinked to original sources

arXiv2026

Stretching and bending of (really) thick elastic plates

The mechanical energy of an elastic plate separates into stretching and bending energies. This is a result for asymptotically thin plates, but it is often a surprisingly accurate approximation for thick plates, too. Here, we address this conundrum: We compute the deformations of a thick elastic plate resulting from imposed, asymptotically small deformations of its midline to discover effective stretching and bending moduli. They soften with increasing plate thickness, but, strikingly, their ratio remains approximately constant. In this way, our calculations provide a justification for applying the thin-plate picture of stretching and bending to thick plates such as biological cell sheets.

cond-mat.soft↗

arXiv2026

Travelling waves of invasion in microbial communities with phenotypic switching

Complex microbial habitats see the spatial competition of different clonal bacterial populations that switch between different phenotypes. Here, we determine the effect of this subpopulation structure on the invasion of one species by another in a minimal model of two competing species: one species switches, both stochastically and in response to its competitor, to a persister phenotype resilient to competition. Surprisingly, our combined analytical and numerical results show that this phenotypic switching has no effect on the speed of the travelling wave by which the competitors invade the first population. Conversely, we discover that phenotypic switching can speed up the wave by which this population invades their competitors. Our results thus suggest, counterintuitively, that bacterial persistence can be an offensive, rather than defensive ecological strategy.

q-bio.PE↗

arXiv2026

Nonlinear isotropic odd elasticity

The nonconservative elastic responses of active solids have driven a recent explosion of interest in two-dimensional "odd" elasticity: small, linear deformations of these Cauchy elastic solids enable new behaviour absent from classical, passive elasticity. Here, we establish the description of large, nonlinear deformations of isotropic two-dimensional Cauchy elastic solids. We apply our framework to the Rivlin problem, perhaps the simplest problem of elasticity lacking a linear analogue: a square deforms under dead load tractions. Surprisingly, we find that oddness suppresses the bifurcations of a passive Rivlin square. By contrast, we discover that the bifurcations of a three-dimensional Rivlin cube survive oddness even though there is no isotropic, odd linear elasticity in three dimensions. Our results thus form the basis for describing large deformations of active, biological solids while revealing their unexpected nonlinear behaviour that arises even in minimal problems.

cond-mat.soft↗

arXiv2026

A mechanical bifurcation constrains the evolution of cell sheet folding in the family Volvocaceae

The processes of morphogenesis that give rise to the shapes of organs and organisms during development are often driven by mechanical instabilities. Can such mechanical bifurcations also drive or constrain the evolution of these processes in the first place? We discover an instance of these constraints in the green algae of the family Volvocaceae. During their development, their bowl-shaped embryonic cell sheet turns itself inside out. This inversion is driven by a simple wave of cell wedging in the genus Pleodorina (16-128 cells) and more complex programmes of cell shape changes in Volvox (~400-50000 cells). However, no species with intermediate cell numbers (256 cells) have been described. Here, we relate this gap to a mechanical bifurcation: Focusing on the inversion of Pleodorina californica (64 cells), we develop a continuum model, in which the cell shape changes driving inversion appear as changes of the intrinsic curvature of an elastic surface. A mechanical bifurcation in this model predicts that inversion is only possible in a subset of its parameter space. Strikingly, parameters estimated for P. californica fall into this possible subset, but those that we extrapolate to 256 or more cells using allometric observations and a model of cell cleavage in Volvocaceae do not. Our work thus suggests that the more complex inversion strategies of Volvox are an evolutionary necessity to obviate this bifurcation and indicates more broadly how mechanical bifurcations can drive the evolution of morphogenesis.

cond-mat.soft↗

arXiv2025

Elasticity and plasticity of epithelial gap closure

Epiboly, during which a tissue closes around the surface of the egg, pervades animal development. This epithelial gap closure involves cell intercalations at the edge of the gap. Here, inspired by serosa closure in the beetle Tribolium, we study the interplay between these plastic cell rearrangements and the elasticity of the tissue in a minimal continuum model of the closure of a circular gap bounded by a contractile actomyosin cable. We discover two different closure mechanisms at the tissue scale depending on the energy barrier $E_\text{b}$ to and the energy $ΔE$ released by intercalation: If $E_\text{b}\ggΔE$, cells intercalate into the gap to close it. For a fluidised tissue in which $E_\text{b}\llΔE$, however, cells deintercalate from the boundary into the bulk of the tissue, and we reveal an emergent mechanical role of inhomogeneities of the actomyosin cable. Our work thus explains the mechanical role of tissue fluidisation in Tribolium serosa closure and processes of epiboly and wound healing more generally.

cond-mat.soft↗

arXiv2025

Control of lumen morphology by lateral and basal cell surfaces

Across development, the morphology of fluid-filled lumina enclosed by epithelial tissues arises from an interplay of lumen pressure, mechanics of the cell cortex, and cell-cell adhesion. Here, we explore the mechanical basis for the control of this interplay using the shape space of MDCK cysts and the instability of their apical surfaces under tight junction perturbations [Mukenhirn et al., Dev. Cell 59, 2886 (2024)]. We discover that the cysts respond to these perturbations by significantly modulating their lateral and basal tensions, in addition to the known modulations of pressure and apical belt tension. We develop a mean-field three-dimensional vertex model of these cysts that reproduces the experimental shape instability quantitatively. This reveals that the observed increase of lateral contractility is a cellular response that counters the instability. Our work thus shows how regulation of the mechanics of all cell surfaces conspires to control lumen morphology.

cond-mat.soft↗

arXiv2025

Strata of Ecological Coexistence via Grassmannians

We study the Lotka--Volterra system from the perspective of computational algebraic geometry, focusing on equilibria that are both feasible and stable. These conditions stratifies the parameter space in $\mathbb{R}\times\mathbb{R}^{n\times n}$ with the feasible-stable semialgebraic sets. We encode them on the real Grassmannian ${\rm Gr}_{\mathbb{R}}(n,2n)$ via a parameter matrix representation, and use oriented matroid theory to develop an algorithm, combining Grassmann--Pl{ü}cker relations with branching under feasibility and stability constraints. This symbolic approach determines whether a given sign pattern in the parameter space $\mathbb{R}\times\mathbb{R}^{n\times n}$ admits a consistent extension to Pl{ü}cker coordinates. As an application, we establish the impossibility of certain interaction networks, showing that the corresponding patterns admit no such extension satisfying feasibility and stability conditions, through an effective implementation. We complement these results using numerical nonlinear algebra with \texttt{HypersurfaceRegions.jl} to decompose the parameter space and detect rare feasible-stable sign patterns.

math.AG↗

arXiv2025

Geometry of T1 transitions in epithelia

The flows of tissues of epithelial cells often involve T1 transitions. These neighbour exchanges are irreversible rearrangements crossing an energy barrier. Here, by an exact geometric construction, I determine this energy barrier for general, isolated T1 transitions dominated by line tensions. I~show how deviations from regular cell packing reduce this energy barrier, but find that line tension fluctuations increase it on average. By another exact construction, I prove that the nonlinear tensions in vertex models of tissues also resist T1 transitions. My results thus form the basis for coarse-grained understanding of cell neighbour exchanges for continuum descriptions of epithelia.

cond-mat.soft↗

arXiv2025

Euler buckling on curved surfaces

Euler buckling epitomises mechanical instabilities: An inextensible straight elastic line buckles under compression when the compressive force reaches a critical value $F_\ast>0$. Here, we extend this classical, planar instability to the buckling under compression of an inextensible relaxed elastic line on a curved surface. By weakly nonlinear analysis of an asymptotically short elastic line, we reveal that the buckling bifurcation changes fundamentally: The critical force for the lowest buckling mode is $F_\ast=0$ and higher buckling modes disconnect from the undeformed branch to connect in pairs. Solving the buckling problem numerically, we additionally find a new post-buckling instability: A long elastic line on a curved surface snaps through under sufficient compression. Our results thus set the foundations for understanding the buckling instabilities on curved surfaces that pervade the emergence of shape in biology.

cond-mat.soft↗

arXiv2025

A model for boundary-driven tissue morphogenesis

Tissue deformations during morphogenesis can be active, driven by internal processes, or passive, resulting from stresses applied at their boundaries. Here, we introduce the Drosophila hindgut primordium as a model for studying boundary-driven tissue morphogenesis. We characterize its deformations and show that its complex shape changes can be a passive consequence of the deformations of the active regions of the embryo that surround it. First, we find an intermediate characteristic triangular shape in the 3D deformations of the hindgut. We construct a minimal model of the hindgut primordium as an elastic ring deformed by active midgut invagination and germ band extension on an ellipsoidal surface, which robustly captures the symmetry-breaking into this triangular shape. We then quantify the 3D kinematics of the tissue by a set of contours and discover that the hindgut deforms in two stages: an initial translation on the curved embryo surface followed by a rapid breaking of shape symmetry. We extend our model to show that the contour kinematics in both stages are consistent with our passive picture. Our results suggest that the role of in-plane deformations during hindgut morphogenesis is to translate the tissue to a region with anisotropic embryonic curvature and show that uniform boundary conditions are sufficient to generate the observed nonuniform shape change. Our work thus provides a possible explanation for the various characteristic shapes of blastopore-equivalents in different organisms and a framework for the mechanical emergence of global morphologies in complex developmental systems.

physics.bio-ph↗

arXiv2024

(Un)buckling mechanics of epithelial monolayers under compression

When cell sheets fold during development, their apical or basal surfaces constrict and cell shapes approach the geometric singularity in which these surfaces vanish. Here, we reveal the mechanical consequences of this geometric singularity for tissue folding in a minimal vertex model of an epithelial monolayer. In simulations of the buckling of the epithelium under compression and numerical solutions of the corresponding continuum model, we discover an "unbuckling" bifurcation: At large compression, the buckling amplitude can decrease with increasing compression. By asymptotic solution of the continuum equations, we reveal that this bifurcation comes with a large stiffening of the epithelium. Our results thus provide the mechanical basis for absorption of compressive stresses by tissue folds such as the cephalic furrow during germband extension in Drosophila.

cond-mat.soft↗

arXiv2024

Mechanics of poking a cyst

Indentation tests are classical tools to determine material properties. For biological samples such as cysts of cells, however, the observed force-displacement relation cannot be expected to follow predictions for simple materials. Here, by solving the Pogorelov problem of a point force indenting an elastic shell for a purely nonlinear material, we discover that complex material behaviour can even give rise to new scaling exponents in this force-displacement relation. In finite-element simulations, we show that these exponents are surprisingly robust, persisting even for thick shells indented with a sphere. By scaling arguments, we generalise our results to pressurised and pre-stressed shells, uncovering additional new scaling exponents. We find these predicted scaling exponents in the force-displacement relation observed in cyst indentation experiments. Our results thus form the basis for inferring the mechanisms that set the mechanical properties of these biological materials.

cond-mat.soft↗

arXiv2024

Buckling by disordered growth

Buckling instabilities driven by tissue growth underpin key developmental events such as the folding of the brain. Tissue growth is disordered due to cell-to-cell variability, but the effects of this variability on buckling are unknown. Here, we analyse what is perhaps the simplest setup of this problem: the buckling of an elastic rod with fixed ends driven by spatially varying growth. Combining analytical calculations for simple growth fields and numerical sampling of random growth fields, we show that variability can increase as well as decrease the growth threshold for buckling, even when growth variability does not cause any residual stresses. For random growth, we find that the shift of the buckling threshold correlates with spatial moments of the growth field. Our results imply that biological systems can either trigger or avoid buckling by exploiting the spatial arrangement of growth variability.

cond-mat.soft↗

arXiv2023

Cut it out: Out-of-plane stresses in cell sheet folding of Volvox embryos

The folding of cellular monolayers pervades embryonic development and disease. It results from stresses out of the plane of the tissue, often caused by cell shape changes including cell wedging via apical constriction. These local cellular changes need not however be compatible with the global shape of the tissue. Such geometric incompatibilities lead to residual stresses that have out-of-plane components in curved tissues, but the mechanics and function of these out-of-plane stresses are poorly understood, perhaps because their quantification has proved challenging. Here, we overcome this difficulty by combining laser ablation experiments and a mechanical model to reveal that such out-of-plane residual stresses exist and also persist during the inversion of the spherical embryos of the green alga Volvox. We show how to quantify the mechanical properties of the curved tissue from its unfurling on ablation, and reproduce the tissue shape sequence at different developmental timepoints quantitatively by our mechanical model. Strikingly, this reveals not only clear mechanical signatures of out-of-plane stresses associated with cell shape changes away from those regions where cell wedging bends the tissue, but also indicates an adaptive response of the tissue to these stresses. Our results thus suggest that cell sheet folding is guided mechanically not only by cell wedging, but also by out-of-plane stresses from these additional cell shape changes.

cond-mat.soft↗

arXiv2023

Impossible ecologies: Interaction networks and stability of coexistence in ecological communities

Does an ecological community allow stable coexistence? Identifying the general principles that determine the answer to this question is a central problem of theoretical ecology. Random matrix theory approaches have uncovered the general trends of the effect of competitive, mutualistic, and predator-prey interactions between species on stability of coexistence. However, an ecological community is determined not only by the counts of these different interaction types, but also by their network arrangement. This cannot be accounted for in a direct statistical description that would enable random matrix theory approaches. Here, we therefore develop a different approach, of exhaustive analysis of small ecological communities, to show that this arrangement of interactions can influence stability of coexistence more than these general trends. We analyse all interaction networks of $N\leqslant 5$ species with Lotka-Volterra dynamics by combining exact results for $N\leqslant 3$ species and numerical exploration. Surprisingly, we find that a very small subset of these networks are "impossible ecologies", in which stable coexistence is non-trivially impossible. We prove that the possibility of stable coexistence in general ecologies is determined by similarly rare "irreducible ecologies". By random sampling of interaction strengths, we then show that the probability of stable coexistence varies over many orders of magnitude even in ecologies that differ only in the network arrangement of identical ecological interactions. Finally, we demonstrate that our approach can reveal the effect of evolutionary or environmental perturbations of the interaction network. Overall, this work reveals the importance of the full structure of the network of interactions for stability of coexistence in ecological communities.

q-bio.PE↗

arXiv2022

Stabilization of Microbial Communities by Responsive Phenotypic Switching

Clonal microbes can switch between different phenotypes and recent theoretical work has shown that stochastic switching between these subpopulations can stabilize microbial communities. This phenotypic switching need not be stochastic, however, but could also be in response to environmental factors, both biotic and abiotic. Here, motivated by the bacterial persistence phenotype, we explore the ecological effects of such responsive switching by analyzing phenotypic switching in response to competing species. We show that the stability of microbial communities with responsive switching differs generically from that of communities with stochastic switching only. To understand the mechanisms by which responsive switching stabilizes coexistence, we go on to analyze simple two-species models. Combining exact results and numerical simulations, we extend the classical stability results for the competition of two species without phenotypic variation to the case in which one species switches, stochastically and responsively, between two phenotypes. In particular, we show that responsive switching can stabilize coexistence even when stochastic switching on its own does not affect the stability of the community.

q-bio.PE↗

arXiv2021

Turing's diffusive threshold in random reaction-diffusion systems

Turing instabilities of reaction-diffusion systems can only arise if the diffusivities of the chemical species are sufficiently different. This threshold is unphysical in most systems with $N=2$ diffusing species, forcing experimental realizations of the instability to rely on fluctuations or additional nondiffusing species. Here we ask whether this diffusive threshold lowers for $N>2$ to allow "true" Turing instabilities. Inspired by May's analysis of the stability of random ecological communities, we analyze the probability distribution of the diffusive threshold in reaction-diffusion systems defined by random matrices describing linearized dynamics near a homogeneous fixed point. In the numerically tractable cases $N\leqslant 6$, we find that the diffusive threshold becomes more likely to be smaller and physical as $N$ increases and that most of these many-species instabilities cannot be described by reduced models with fewer species.

cond-mat.soft↗

arXiv2021

Comment on "Faceting and Flattening of Emulsion Droplets: A Mechanical Model"

García-Aguilar et al. [Phys. Rev. Lett 126, 038001 (2021)] have shown that the deformations of "shape-shifting droplets" are consistent with an elastic model, that, unlike previous models, includes the intrinsic curvature of the frozen surfactant layer. In this Comment, we show that the interplay between surface tension and intrinsic curvature in their model is in fact mathematically equivalent to a physically very different phase-transition mechanism of the same process that we developed previously [Phys. Rev. Lett. 118, 088001 (2017); Phys. Rev. Res. 1, 023017 (2019)]. The mathematical models cannot therefore distinguish between the two mechanisms, and hence it is not possible to claim that one mechanism underlies all observed shape-shifting phenomena without a much more detailed comparison of experiment and theory.

cond-mat.soft↗