No Arabic abstract
Inspired by active shape morphing in developing tissues and biomaterials, we investigate two generic mechanochemical models where the deformations of a thin elastic sheet are driven by, and in turn affect, the concentration gradients of a chemical signal. We develop numerical methods to study the coupled elastic deformations and chemical concentration kinetics, and illustrate with computations the formation of different patterns depending on shell thickness, strength of mechanochemical coupling and diffusivity. In the first model, the sheet curvature governs the production of a contractility inhibitor and depending on the threshold in the coupling, qualitatively different patterns occur. The second model is based on the stress--dependent activity of myosin motors, and demonstrates how the concentration distribution patterns of molecular motors are affected by the long-range deformations generated by them. Since the propagation of mechanical deformations is typically faster than chemical kinetics (of molecular motors or signaling agents that affect motors), we describe in detail and implement a numerical method based on separation of timescales to effectively simulate such systems. We show that mechanochemical coupling leads to long-range propagation of patterns in disparate systems through elastic instabilities even without the diffusive or advective transport of the chemicals.
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.
Morphogenetic dynamics of tissue sheets require coordinated cell shape changes regulated by global patterning of mechanical forces. Inspired by such biological phenomena, we propose a minimal mechanochemical model based on the notion that cell shape changes are induced by diffusible biomolecules that influence tissue contractility in a concentration-dependent manner -- and whose concentration is in turn affected by the macroscopic tissue shape. We perform computational simulations of thin shell elastic dynamics to reveal propagating chemical and three-dimensional deformation patterns arising due to a sequence of buckling instabilities. Depending on the concentration threshold that actuates cell shape change, we find qualitatively different patterns. The mechanochemically coupled patterning dynamics are distinct from those driven by purely mechanical or purely chemical factors. Using numerical simulations and theoretical arguments, we analyze the elastic instabilities that result from our model and provide simple scaling laws to identify wrinkling morphologies.
We consider three-dimensional reshaping of thin nemato-elastic sheets containing half-charged defects upon nematic-isotropic transition. Gaussian curvature, that can be evaluated analytically when the nematic texture is known, differs from zero in the entire domain and has a dipole or hexapole singularity, respectively, at defects of positive or negative sign. The latter kind of defects appears in not simply connected domains. Three-dimensional shapes dependent on boundary anchoring are obtained with the help of finite element computations.
We show that a viscoelastic thin sheet driven out of equilibrium by active structural remodelling develops a rich variety of shapes as a result of a competition between viscous relaxation and activity. In the regime where active processes are faster than viscoelastic relaxation, wrinkles that are formed due to remodelling are unable to relax to a configuration that minimises the elastic energy and the sheet is inherently out of equilibrium. We argue that this non-equilibrium regime is of particular interest in biology as it allows the system to access morphologies that are unavailable if restricted to the adiabatic evolution between configurations that minimise the elastic energy alone. Here, we introduce activity using the formalism of evolving target metric and showcase the diversity of wrinkling morphologies arising from out of equilibrium dynamics.
Thin elastic sheets supported on compliant media form wrinkles under lateral compression. Since the lateral pressure is coupled to the sheets deformation, varying it periodically in time creates a parametric excitation. We study the resulting parametric resonance of wrinkling modes in sheets supported on semi-infinite elastic or viscoelastic media, at pressures smaller than the critical pressure of static wrinkling. We find distinctive behaviors as a function of excitation amplitude and frequency, including (a) a different dependence of the dynamic wrinkle wavelength on sheet thickness compared to the static wavelength; and (b) a discontinuous decrease of the wrinkle wavelength upon increasing excitation frequency at sufficiently large pressures. In the case of a viscoelastic substrate, resonant wrinkling requires crossing a threshold of excitation amplitude. The frequencies for observing these phenomena in relevant experimental systems are of the order of a kilohertz and above. We discuss experimental implications of the results.