Active Cell Nematics: Architectures and flows

When cultured in monolayers, spindle-shaped cells such as NIH-3t3 fibroblasts form domains of common orientation whose characteristic size (~ 500 µm) is very large compared to a cell size. These domains don’t fuse because of the presence of intrinsic topological defects characteristic of these 2D nematic phases. Confining these fibroblasts in mesoscale stripes whose width is smaller than this length results in a defect-free nematic ordering whose director aligns with the stripe’s direction. However, in the same confinement condition, more active cell types such as myoblasts adopt a more complex nematic architecture by spontaneously orienting at a finite angle with respect to the stripe direction, and developing a shear flow. This situation is reminiscent of in vivo observations where cancer cells escaping collectively from a tumor can locally migrate in antiparallel directions within the same strand. Cell types characterized by an even higher activity show hallmarks of turbulence. Confining the cells in circular domains imposes a topological charge that results in a pair of defects whose position indicates that, at high cell density, activity is eventually overcome by friction with the underlying substrate. Finally, myoblasts don’t remain as monolayers but eventually form multilayers. We show that this multilayering process is initiated at defects and is made possible by the secretion of Extra Cellular Matrix by the cells. Because of the architecture of the cells near the core of the defect, successive layers are perpendicularly oriented as it is often the case for muscle tissues in vivo.

Ref: Duclos et al. Soft Matt. (2014) ; Duclos et al. Nat. Phys. (2017) ; Duclos et al. Nat. Phys. (2018) ; Blanch Mercader et al. Phys. Rev. Lett. (2018)