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The Random First-Order Transition (RFOT) theory predicts that transport proceeds by the cooperative movement of particles in domains, whose sizes increase as a liquid is compressed above a characteristic volume fraction, ϕd. The rounded dynamical transition around ϕd, which signals a crossover to activated transport, is accompanied by a growing correlation length that is predicted to diverge at the thermodynamic glass transition density (>ϕd). Simulations and imaging experiments probed the single particle dynamics of mobile particles in response to pinning all the particles in a semi-infinite space or randomly pinning (RP) a fraction of particles in a liquid at equilibrium. The extracted dynamic length increases non-monotonically with a peak around ϕd, which not only depends on the pinning method but is also different from ϕd of the actual liquid. This finding is at variance with the results obtained using the small wavelength limit of a four-point structure factor for unpinned systems. To obtain a consistent picture of the growth of the dynamic length, one that is impervious to the use of RP, we introduce a multiparticle structure factor, Smpc(q,t), that probes collective dynamics. The collective dynamical length, calculated from the small wave vector limit of Smpc(q,t), increases monotonically as a function of the volume fraction in a glass-forming binary mixture of charged colloidal particles in both unpinned and pinned systems. This prediction, which also holds in the presence of added monovalent salt, may be validated using imaging experiments. 

A recent experiment on zebrafish blastoderm morphogenesis showed that the viscosity (η) of a non-confluent embryonic tissue grows sharply until a critical cell packing fraction (ϕ_S). The increase inηup toϕ_Sis similar to the behavior observed in several glass-forming materials, which suggests that the cell dynamics is sluggish or glass-like. Surprisingly,ηis a constant aboveϕ_S. To determine the mechanism of this unusual dependence ofηonϕ, we performed extensive simulations using an agent-based model of a dense non-confluent two-dimensional tissue. We show that polydispersity in the cell size, and the propensity of the cells to deform, results in the saturation of the available free area per cell beyond a critical packing fraction. Saturation in the free space not only explains the viscosity plateau aboveϕ_Sbut also provides a relationship between equilibrium geometrical packing to the dramatic increase in the relaxation dynamics. 

The growth of a tissue, which depends on cell–cell interactions and biologically relevant processes such as cell division and apoptosis, is regulated by a mechanical feedback mechanism. We account for these effects in a minimal two-dimensional model in order to investigate the consequences of mechanical feedback, which is controlled by a critical pressure, p c . A cell can only grow and divide if its pressure, due to interaction with its neighbors, is less than p c . Because temperature is not a relevant variable, the cell dynamics is driven by self-generated active forces (SGAFs) that arise due to cell division. We show that even in the absence of intercellular interactions, cells undergo diffusive behavior. The SGAF-driven diffusion is indistinguishable from the well-known dynamics of a free Brownian particle at a fixed finite temperature. When intercellular interactions are taken into account, we find persistent temporal correlations in the force–force autocorrelation function (FAF) that extends over a timescale of several cell division times. The time-dependence of the FAF reveals memory effects, which increases as p c increases. The observed non-Markovian effects emerge due to the interplay of cell division and mechanical feedback and are inherently a non-equilibrium phenomenon.