rigidity
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Making a Mesh of Things: Using Network Models to Understand the Mechanics of Heterogeneous Tissues
Networks of stiff biopolymers are an omnipresent structural motif in cells and tissues. A prominent modeling framework for describing biopolymer network mechanics is rigidity percolation theory. This theory describes model networks as nodes joined by randomly placed, springlike bonds. Increasing the amount of bonds in a network results in an abrupt, dramatic increase in elastic moduli above a certain threshold – an example of a mechanical phase transition. While homogeneous networks are well studied, many tissues are made of disparate components and exhibit spatial fluctuations in the concentrations of their constituents. In this talk, I will first discuss recent work in which we explained the structural basis of the shear mechanics of healthy and chemically degraded cartilage by coupling a rigidity percolation framework with a background gel. Our model takes into account collagen concentration, as well as the concentration of peptidoglycans in the surrounding polyelectrolyte gel, to produce a structureproperty relationship that describes the shear mechanics of both sound and diseased cartilage. I will next discuss the introduction of structural correlation in constructing networks, such that sparse and dense patches emerge. I find moderate correlation allows a network to become rigid with fewer bonds, while this benefit is partly erased by excessive correlation. We explain this phenomenon through analysis of the spatial fluctuations in strained networks’ displacement fields. Finally, I will address our work’s implications for non-invasive diagnosis of pathology, as well as rational design of prostheses and novel soft materials.
Tissue fluidization at the onset of zebrafish gastrulation
Embryo morphogenesis is impacted by dynamic changes in tissue material properties, which have been proposed to occur via processes akin phase transitions (PTs). Here, we show that rigidity percolation provides a simple and robust theoretical framework to predict material/structural PTs of embryonic tissues from local cell connectivity. By using percolation theory, combined with directly monitoring dynamic changes in tissue rheology and cell contact mechanics, we demonstrate that the zebrafish blastoderm undergoes a genuine rigidity PT, brought about by a small reduction in adhesion-dependent cell connectivity below a critical value. We quantitatively predict and experimentally verify hallmarks of PTs, including power-law exponents and associated discontinuities of macroscopic observables at criticality. Finally, we show that this uniform PT depends on blastoderm cells undergoing meta-synchronous divisions causing random and, consequently, uniform changes in cell connectivity. Collectively, our theoretical and experimental findings reveal the structural basis of material PTs in an organismal context.
Bend, slip, or break?
Rigidity is the ability of a system to resist imposed stresses before ultimately undergoing failure. However, disordered materials often contain both rigid and floppy subregions that complicate the utility of taking system-wide averages. I will talk about 3 frameworks capable of connecting the internal structure of disordered materials to their rigidity and/or failure under loading, and describe how my collaborators and I have applied these frameworks to laboratory data on laser-cut lattices and idealized granular materials. These are, in order of increasing physics content: (1) centrality within an adjacency matrix describing its connectivity, (2) Maxwell constraint counting on the full network of frictional contact forces, and (3) the vibrational modes of a synthetic dynamical matrix (Hessian). The first two rely primarily on topology, and the second two contrast the utility of considering interparticle forces (Coulomb failure) vs. the energy landscape. All three methods, while successfully elucidating the origins of rigidity and brittle vs. ductile failure, also provide interesting counterpoints regarding how much information is enough to make predictions.
“Rigidity and Fluidity in Biological Tissue”
The coordinated migration of groups of cells underlies many biological processes, including embryo development, wound healing and cancer metastasis. In many of these situations, tissues are able to tune themselves between liquid-like states, where cells flow collectively as in a liquid, and solid-like states that can support shear stresses. In this talk I will describe mesoscopic models of cell assemblies inspired by active matter physics to examine the roles of cell motility, cell crowding and the interplay of contractility and adhesion in controlling the rheological state of biological tissue.
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