Molecular-scale substrate anisotropy, crowding and division drive collective behaviours in cell monolayers.

The ability of cells to reorganize in response to external stimuli is important in areas ranging from morphogenesis to tissue engineering. While nematic order is common in biological tissues, it typically only extends to small regions of cells interacting via steric repulsion. On isotropic substrates, elongated cells can co-align due to steric effects, forming ordered but randomly oriented finite-size domains. However, we have discovered that flat substrates with nematic order can induce global nematic alignment of dense, spindle-like cells, thereby influencing cell organization and collective motion and driving alignment on the scale of the entire tissue. Remarkably, single cells are not sensitive to the substrate's anisotropy. Rather, the emergence of global nematic order is a collective phenomenon that requires both steric effects and molecular-scale anisotropy of the substrate. To quantify the rich set of behaviours afforded by this system, we analyse velocity, positional and orientational correlations for several thousand cells over days. The establishment of global order is facilitated by enhanced cell division along the substrate's nematic axis, and associated extensile stresses that restructure the cells' actomyosin networks. Our work provides a new understanding of the dynamics of cellular remodelling and organization among weakly interacting cells.

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 .