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Collective response to external directional cues like electric fields helps guide tissue development, regeneration, and wound healing. In this study we focus on the impact of anisotropy in cell shape and local cell alignment on the collective response to electric fields. We model elongated cells that have a different accuracy sensing the field depending on their orientation with respect to the field. With this framework, we assume cells are better sensors if they can align their long axes perpendicular to the field. Elongated cells often line up with their long axes in the same direction — “nematic order” – does a nematic cell-cell interaction allow groups of cells to share information about their orientation to sense fields more accurately? We use simulations of a simple model to show that if cells orient themselves perpendicular to their average velocity, alignment of a cell’s long axis to its nearest neighbors’ orientation can in some circumstances enhance the directional response to electric fields. We also show that cell-cell adhesion modulates the accuracy of cells in the group. 

Collective movement and organization of cell monolayers are important for wound healing and tissue development. Recent experiments highlighted the importance of liquid crystal order within these layers, suggesting that +1 topological defects have a role in organizing tissue morphogenesis. We study fibroblast organization, motion, and proliferation on a substrate with micron-sized ridges that induce +1 and −1 topological defects using simulation and experiment. We model cells as self-propelled deformable ellipses that interact via a Gay–Berne potential. Unlike earlier work on other cell types, we see that density variation near defects is not explained by collective migration. We propose instead that fibroblasts have different division rates depending on their area and aspect ratio. This model captures key features of our previous experiments: the alignment quality worsens at high cell density and, at the center of the +1 defects, cells can adopt either highly anisotropic or primarily isotropic morphologies. Experiments performed with different ridge heights confirm a prediction of this model: Suppressing migration across ridges promotes higher cell density at the +1 defect. Our work enables a mechanism for tissue patterning using topological defects without relying on cell migration.