Julia Yeomans OBE FRS

Abstract:

We investigate channel-confined, nematic liquid crystals using the Beris–Edwards model of nematohydrodynamics. Using strong homeotropic anchoring at the walls, we find multistability, i.e. multiple coexisting states where the uniform nematic state coexists with states having spatially varying scalar nematic order and director fields. When a pressure gradient is applied, flows develop, and the inherent multistability of the system organises a variety of complex dynamics. For low pressure gradients, steady flows are established, and the director fields that emerge from the multistable states at equilibrium correspond to Bowser and Dowser configurations similar to those reported in experiments. An increasing pressure gradient destabilises steady Bowser and Dowser flow states sequentially, leading to unsteady periodic and chaotic regimes featuring cyclical topological transitions, pulsating flows, advecting defects and spatiotemporal chaos. These findings demonstrate that modest variations in the scalar nematic order, as captured by the Beris–Edwards model, can qualitatively modify equilibrium structures and give rise to complex non-equilibrium behaviour in confined nematics – contrasting with the Ericksen–Leslie model, which assumes a constant scalar order parameter. Our key model predictions – multistability, periodically oscillating states and advecting defect-mediated turbulence – can be experimentally investigated in pressure-driven channel flows of nematic fluids.

Abstract:

Although cell monolayers typically remain confluent, they can spontaneously develop persistent holes as a result of collective cellular motion. Recent studies on MDCK monolayers cultured on soft substrates have revealed that cells can align to create regions of local nematic order, and topological defects that generate localised mechanical stresses which can spontaneously trigger hole formation. To investigate this process, we develop a continuum multi-phase field model that incorporates internal dissipation and active dipolar forces that drive cell shape anisotropy. Our simulations show that reducing substrate friction enhances cell-cell velocity correlations. In the low-friction regime, topological defects generate spiral flow patterns that concentrate stress and can trigger hole formation. By contrast, in the high-friction regime, holes do not nucleate. We further demonstrate that the number and stability of the holes—whether they close or persist—depends on both substrate friction and cellular activity, through a non-dimensional friction number. These findings highlight the importance of internal dissipation in modelling collective cell motion and the critical role of collective dynamics in maintaining tissue integrity.

Abstract:

Active matter—for example, bacteria, cells, tissues, and microtubule-motor suspensions—internally generates stresses and flows. How these are communicated to their environments remains an open question central to interpreting experimental observations and emergent dynamics. To investigate the impact of active systems on their surroundings, we introduce a model that couples an active nematic fluid to an isotropic substrate fluid via friction. We numerically show that as the active layer develops turbulence, the substrate inherits the chaotic behavior, exhibiting a novel form of turbulence driven by locally generated stochastic forcing from the active layer. In particular, the short-length-scale flow structures in the active layer are filtered out, so the system behaves as a de facto low-pass filter. We derive the transfer function between the two layers analytically and use it to predict the large-q decay of the substrate energy spectrum and to investigate how tensorial quantities, such as the strain rate and the active stresses, are transmitted between the active layer and the substrate. Our analysis agrees with recent experiments measuring velocity-velocity correlations in mixtures of active and passive microtubules, and it may have implications for traction force microscopy measurements in cellular layers.