Design rules for controlling active topological defects.

Topological defects play a central role in the physics of many materials, including magnets, superconductors, and liquid crystals. In active fluids, defects become autonomous particles that spontaneously propel from internal active stresses and drive chaotic flows stirring the fluid. The intimate connection between defect textures and active flow suggests that properties of active materials can be engineered by controlling defects, but design principles for their spatiotemporal control remain elusive. Here, we propose a symmetry-based additive strategy for using elementary activity patterns, as active topological tweezers, to create, move, and braid such defects. By combining theory and simulations, we demonstrate how, at the collective level, spatial activity gradients act like electric fields which, when strong enough, induce an inverted topological polarization of defects, akin to a negative susceptibility dielectric. We harness this feature in a dynamic setting to collectively pattern and transport interacting active defects. Our work establishes an additive framework to sculpt flows and manipulate active defects in both space and time, paving the way to design programmable active and living materials for transport, memory, and logic.

Cell Division and Motility Enable Hexatic Order in Biological Tissues.

Biological tissues transform between solid- and liquidlike states in many fundamental physiological events. Recent experimental observations further suggest that in two-dimensional epithelial tissues these solid-liquid transformations can happen via intermediate states akin to the intermediate hexatic phases observed in equilibrium two-dimensional melting. The hexatic phase is characterized by quasi-long-range (power-law) orientational order but no translational order, thus endowing some structure to an otherwise structureless fluid. While it has been shown that hexatic order in tissue models can be induced by motility and thermal fluctuations, the role of cell division and apoptosis (birth and death) has remained poorly understood, despite its fundamental biological role. Here we study the effect of cell division and apoptosis on global hexatic order within the framework of the self-propelled Voronoi model of tissue. Although cell division naively destroys order and active motility facilitates deformations, we show that their combined action drives a liquid-hexatic-liquid transformation as the motility increases. The hexatic phase is accessed by the delicate balance of dislocation defect generation from cell division and the active binding of disclination-antidisclination pairs from motility. We formulate a mean-field model to elucidate this competition between cell division and motility and the consequent development of hexatic order.

The role of non-affine deformations in the elastic behavior of the cellular vertex model.

The vertex model of epithelia describes the apical surface of a tissue as a tiling of polygonal cells, with a mechanical energy governed by deviations in cell shape from preferred, or target, area, A0, and perimeter, P0. The model exhibits a rigidity transition driven by geometric incompatibility as tuned by the target shape index, . For with p*(6) the perimeter of a regular hexagon of unit area, a cell can simultaneously attain both the preferred area and preferred perimeter. As a result, the tissue is in a mechanically soft compatible state, with zero shear and Young's moduli. For p0 < p*(6), it is geometrically impossible for any cell to realize the preferred area and perimeter simultaneously, and the tissue is in an incompatible rigid solid state. Using a mean-field approach, we present a complete analytical calculation of the linear elastic moduli of an ordered vertex model. We analyze a relaxation step that includes non-affine deformations, leading to a softer response than previously reported. The origin of the vanishing shear and Young's moduli in the compatible state is the presence of zero-energy deformations of cell shape. The bulk modulus exhibits a jump discontinuity at the transition and can be lower in the rigid state than in the fluid-like state. The Poisson's ratio can become negative which lowers the bulk and Young's moduli. Our work provides a unified treatment of linear elasticity for the vertex model and demonstrates that this linear response is protocol-dependent.

Spontaneous Tilt of Single-Clamped Thermal Elastic Sheets.

Very thin elastic sheets, even at zero temperature, exhibit nonlinear elastic response by virtue of their dominant bending modes. Their behavior is even richer at finite temperature. Here, we use molecular dynamics to study the vibrations of a thermally fluctuating two-dimensional elastic sheet with one end clamped at its zero-temperature length. We uncover a tilted phase in which the sheet fluctuates about a mean configuration inclined with respect to the horizontal, thus breaking reflection symmetry. We determine the phase behavior as a function of the aspect ratio of the sheet and the temperature. We show that tilt may be viewed as a type of transverse buckling instability induced by clamping coupled to thermal fluctuations and develop an analytic model that predicts the tilted and untilted regions of the phase diagram. Qualitative agreement is found with the molecular dynamics simulations. Unusual response driven by control of purely geometric quantities like the aspect ratio, as opposed to external fields, offers a very rich playground for two-dimensional mechanical metamaterials.

Fluctuations can induce local nematic order and extensile stress in monolayers of motile cells.

Recent experiments in various cell types have shown that two-dimensional tissues often display local nematic order, with evidence of extensile stresses manifest in the dynamics of topological defects. Using a mesoscopic model where tissue flow is generated by fluctuating traction forces coupled to the nematic order parameter, we show that the resulting tissue dynamics can spontaneously produce local nematic order and an extensile internal stress. A key element of the model is the assumption that in the presence of local nematic alignment, cells preferentially crawl along the nematic axis, resulting in anisotropy of fluctuations. Our work shows that activity can drive either extensile or contractile stresses in tissue, depending on the relative strength of the contractility of the cortical cytoskeleton and tractions by cells on the extracellular matrix.

Shape and size changes of adherent elastic epithelia.

Epithelial tissues play a fundamental role in various morphogenetic events during development and early embryogenesis. Although epithelial monolayers are often modeled as two-dimensional (2D) elastic surfaces, they distinguish themselves from conventional thin elastic plates in three important ways- the presence of an apical-basal polarity, spatial variability of cellular thickness, and their nonequilibrium active nature. Here, we develop a minimal continuum model of a planar epithelial tissue as an active elastic material that incorporates all these features. We start from a full three-dimensional (3D) description of the tissue and derive an effective 2D model that captures, through the curvature of the apical surface, both the apical-basal asymmetry and the spatial geometry of the tissue. Crucially, variations of active stresses across the apical-basal axis lead to active torques that can drive curvature transitions. By identifying four distinct sources of activity, we find that bulk active stresses arising from actomyosin contractility and growth compete with boundary active tensions due to localized actomyosin cables and lamellipodial activity to generate the various states spanning the morphospace of a planar epithelium. Our treatment hence unifies 3D shape deformations through the coupled mechanics of apical curvature change and in-plane expansion/contraction of substrate-adhered tissues. Finally, we discuss the implications of our results for some biologically relevant processes such as tissue folding at the onset of lumen formation.

Erratum: Geometric Frustration and Solid-Solid Transitions in Model 2D Tissue [Phys. Rev. Lett. 120, 268105 (2018)].

This corrects the article DOI: 10.1103/PhysRevLett.120.268105.

Kirigami Mechanics as Stress Relief by Elastic Charges.

We develop a geometric approach to understand the mechanics of perforated thin elastic sheets, using the method of strain-dependent image elastic charges. This technique recognizes the buckling response of a hole under an external load as a geometrically tuned mechanism of stress relief. We use a diagonally pulled square paper frame as a model system to quantitatively test and validate our approach. Specifically, we compare nonlinear force-extension curves and global displacement fields in theory and experiment. We find a strong softening of the force response accompanied by curvature localization at the inner corners of the buckled frame. Counterintuitively, though in complete agreement with our theory, for a range of intermediate hole sizes, wider frames are found to buckle more easily than narrower ones. Upon extending these ideas to many holes, we demonstrate that interacting elastic image charges can provide a useful kirigami design principle to selectively relax stresses in elastic materials.

Non-uniform curvature and anisotropic deformation control wrinkling patterns on tori.

We investigate wrinkling patterns in a tri-layer torus consisting of an expanding thin outer layer, an intermediate soft layer and an inner core with a tunable shear modulus, inspired by pattern formation in developmental biology, such as follicle pattern formation during the development of chicken embryos. We show from large-scale finite element simulations that hexagonal wrinkling patterns form for stiff cores whereas stripe wrinkling patterns develop for soft cores. Hexagons and stripes co-exist to form hybrid patterns for cores with intermediate stiffness. The governing mechanism for the pattern transition is that the stiffness of the inner core controls the degree to which the major radius of the torus expands - this has a greater effect on deformation in the long direction as compared to the short direction of the torus. This anisotropic deformation alters stress states in the outer layer which change from biaxial (preferred hexagons) to uniaxial (preferred stripes) compression as the core stiffness is reduced. As the outer layer continues to expand, stripe and hexagon patterns will evolve into zigzags and segmented labyrinths, respectively. Stripe wrinkles are observed to initiate at the inner surface of the torus while hexagon wrinkles start from the outer surface as a result of curvature-dependent stresses in the torus. We further discuss the effects of elasticities and geometries of the torus on the wrinkling patterns.

Defect Unbinding in Active Nematics.

We formulate the statistical dynamics of topological defects in the active nematic phase, formed in two dimensions by a collection of self-driven particles on a substrate. An important consequence of the nonequilibrium drive is the spontaneous motility of strength +1/2 disclinations. Starting from the hydrodynamic equations of active nematics, we derive an interacting particle description of defects that includes active torques. We show that activity, within perturbation theory, lowers the defect-unbinding transition temperature, determining a critical line in the temperature-activity plane that separates the quasi-long-range ordered (nematic) and disordered (isotropic) phases. Below a critical activity, defects remain bound as rotational noise decorrelates the directed dynamics of +1/2 defects, stabilizing the quasi-long-range ordered nematic state. This activity threshold vanishes at low temperature, leading to a reentrant transition. At large enough activity, active forces always exceed thermal ones and the perturbative result fails, suggesting that in this regime activity will always disorder the system. Crucially, rotational diffusion being a two-dimensional phenomenon, defect unbinding cannot be described by a simplified one-dimensional model.

Geometric Frustration and Solid-Solid Transitions in Model 2D Tissue.

We study the mechanical behavior of two-dimensional cellular tissues by formulating the continuum limit of discrete vertex models based on an energy that penalizes departures from a target area A_{0} and a target perimeter P_{0} for the component cells of the tissue. As the dimensionless target shape index s_{0}=(P_{0}/sqrt[A_{0}]) is varied, we find a transition from a soft elastic regime for a compatible target perimeter and area to a stiffer nonlinear elastic regime frustrated by geometric incompatibility. We show that the ground state in the soft regime has a family of degenerate solutions associated with zero modes for the target area and perimeter. The onset of geometric incompatibility at a critical s_{0}^{c} lifts this degeneracy. The resultant energy gap leads to a nonlinear elastic response distinct from that obtained in classical elasticity models. We draw an analogy between cellular tissues and anelastic deformations in solids.

Topology and ground-state degeneracy of tetrahedral smectic vesicles.

Chemical design of block copolymers makes it possible to create polymer vesicles with tunable microscopic structure. Here we focus on a model of a vesicle made of smectic liquid-crystalline block copolymers at zero temperature. The vesicle assumes a faceted tetrahedral shape and the smectic layers arrange in a stack of parallel straight lines with topological defects localized at the vertices. We counted the number of allowed states at [Formula: see text]. For any fixed shape, we found a two-dimensional countable degeneracy in the smectic pattern depending on the tilt angle between the smectic layers and the edge of the tetrahedral shell. For most values of the tilt angle, the smectic layers contain spiral topological defects. The system can spontaneously break chiral symmetry when the layers organize into spiral patterns, composed of a bound pair of +1/2 disclinations. Finally, we suggest possible applications of tetrahedral smectic vesicles in the context of functionalizing defects and the possible consequences of the spiral structures for the rigidity of the vesicle.

Defect driven shapes in nematic droplets: analogies with cell division.

Building on the striking similarity between the structure of the spindle during mitosis in living cells and nematic textures in confined liquid crystals, we use a continuum model of two-dimensional nematic liquid crystal droplets to examine the physical aspects of cell division. The model investigates the interplay between bulk elasticity of the microtubule assembly, described as a nematic liquid crystal, and surface elasticity of the cell cortex, modeled as a bounding flexible membrane, in controlling cell shape and division. The centrosomes at the spindle poles correspond to the cores of the topological defects required to accommodate nematic order in a closed geometry. We map out the progression of both healthy bipolar and faulty multi-polar division as a function of an effective parameter that incorporates active processes and controls centrosome separation. A robust prediction, independent of energetic considerations, is that the transition from a single cell to daughters cells occurs at critical value of this parameter. Our model additionally suggests that microtubule anchoring at the cell cortex may play an important role for successful bipolar division. This can be tested experimentally by regulating microtubule anchoring.

Morphology of nematic and smectic vesicles.

Recent experiments on vesicles formed from block copolymers with liquid-crystalline side chains reveal a rich variety of vesicle morphologies. The additional internal order ("structure") developed by these self-assembled block copolymer vesicles can lead to significantly deformed vesicles as a result of the delicate interplay between two-dimensional ordering and vesicle shape. The inevitable topological defects in structured vesicles of spherical topology also play an essential role in controlling the final vesicle morphology. Here we develop a minimal theoretical model for the morphology of the membrane structure with internal nematic/smectic order. Using both analytic and numerical approaches, we show that the possible low free energy morphologies include nano-size cylindrical micelles (nano-fibers), faceted tetrahedral vesicles, and ellipsoidal vesicles, as well as cylindrical vesicles. The tetrahedral vesicle is a particularly fascinating example of a faceted liquid-crystalline membrane. Faceted liquid vesicles may lead to the design of supramolecular structures with tetrahedral symmetry and new classes of nano-carriers.

Fractionalization of interstitials in curved colloidal crystals.

Understanding the effect of curvature and topological frustration in crystals yields insights into the fragility of the ordered state. For instance, a one-dimensional crystal of identical charged particles can accommodate an extra particle (interstitial) if all the particle positions are readjusted, yet in a planar hexagonal crystal interstitials remain trapped between lattice sites and diffuse by hopping. Using optical tweezers operated independently of three-dimensional imaging, we inserted interstitials in a lattice of similar colloidal particles sitting on flat or curved oil/glycerol interfaces, and imaged the ensuing dynamics. We find that, unlike in flat space, the curved crystals self-heal through a collective particle rearrangement that redistributes the increased density associated with the interstitial. This process can be interpreted in terms of the out-of-equilibrium interaction of topological defects with each other and with the underlying curvature. Our observations suggest the existence of particle fractionalization on curved surface crystals.

Defect annihilation and proliferation in active nematics.

Liquid crystals inevitably possess topological defect excitations generated through boundary conditions, through applied fields, or in quenches to the ordered phase. In equilibrium, pairs of defects coarsen and annihilate as the uniform ground state is approached. Here we show that defects in active liquid crystals exhibit profoundly different behavior, depending on the degree of activity and its contractile or extensile character. While contractile systems enhance the annihilation dynamics of passive systems, extensile systems act to drive defects apart so that they swarm around in the manner of topologically well-characterized self-propelled particles. We develop a simple analytical model for the defect dynamics which reproduces the key features of both the numerical solutions and recent experiments on microtubule-kinesin assemblies.

Geometric control of tilt transition dynamics in single-clamped thermalized elastic sheets.

We study the finite-temperature dynamics of thin elastic sheets in a single-clamped cantilever configuration. This system is known to exhibit a tilt transition at which the preferred mean plane of the sheet shifts from horizontal to a plane above or below the horizontal. The resultant thermally roughened two-state (up/down) system possesses rich dynamics on multiple timescales. In the tilted regime a finite-energy barrier separates the spontaneously chosen up state from the inversion-symmetric down state. Molecular dynamics simulations confirm that, over sufficiently long time, such thermalized elastic sheets transition between the two states, residing in each for a finite dwell time. One might expect that temperature is the primary driver for tilt inversion. We find, instead, that the primary control parameter, at fixed tilt order parameter, is the dimensionless and purely geometrical aspect ratio of the clamped width to the total length of the otherwise-free sheet. Using a combination of an effective mean-field theory and Kramers' theory, we derive the transition rate and examine its asymptotic behavior. At length scales beyond a material-dependent thermal length scale, renormalization of the elastic constants qualitatively modifies the temperature response. In particular, the transition is suppressed by thermal fluctuations, enhancing the robustness of the tilted state. We check and supplement these findings with further molecular dynamics simulations for a range of aspect ratios and temperatures.

Active cell divisions generate fourfold orientationally ordered phase in living tissue.

Morphogenesis, the process through which genes generate form, establishes tissue-scale order as a template for constructing the complex shapes of the body plan. The extensive growth required to build these ordered substrates is fuelled by cell proliferation, which, naively, should destroy order. Understanding how active morphogenetic mechanisms couple cellular and mechanical processes to generate order-rather than annihilate it-remains an outstanding question in animal development. We show that cell divisions are the primary drivers of tissue flow, leading to a fourfold orientationally ordered phase. Waves of anisotropic cell proliferation propagate across the embryo with precise patterning. Defects introduced into the nascent lattice by cell divisions are moved out of the tissue bulk towards the boundary by subsequent divisions. Specific cell proliferation rates and orientations enable cell divisions to organize rather than fluidize the tissue. We observe this using live imaging and tissue cartography to analyse the dynamics of fourfold tissue ordering in the trunk segmental ectoderm of the crustacean Parhyale hawaiensis beginning 72 h after egg lay. The result is a robust, active mechanism for generating global orientational order in a non-equilibrium system that sets the stage for the subsequent development of shape and form.

The electric double layer structure around charged spherical interfaces.

We derive a formally simple approximate analytical solution to the Poisson-Boltzmann equation for the spherical system via a geometric mapping. Its regime of applicability in the parameter space of the spherical radius and the surface potential is determined, and its superiority over the linearized solution is demonstrated.

Flow around topological defects in active nematic films.

We study the active flow around isolated defects and the self-propulsion velocity of + 1 / 2 defects in an active nematic film with both viscous dissipation (with viscosity η ) and frictional damping Γ with a substrate. The interplay between these two dissipation mechanisms is controlled by the hydrodynamic dissipation length ℓ d = η / Γ that screens the flows. For an isolated defect, in the absence of screening from other defects, the size of the shear vorticity around the defect is controlled by the system size R . In the presence of friction that leads to a finite value of ℓ d , the vorticity field decays to zero on the lengthscales larger than ℓ d . We show that the self-propulsion velocity of + 1 / 2 defects grows with R in small systems where R < ℓ d , while in the infinite system limit or when R ≫ ℓ d , it approaches a constant value determined by ℓ d .