Abstract

Biological tissues are composed of various cell types working cooperatively to perform their respective function within organs and the whole body. During development, embryogenesis followed by histogenesis relies on orchestrated division, death, differentiation and collective movements of cellular constituents. These cells are anchored to each other and/or the underlying substrate through adhesion complexes and they regulate force generation by active cytoskeleton remodeling. The resulting changes in contractility at the level of each single cell impact tissue architecture and remodeling by triggering changes in cell shape, cell movement and remodeling of the surrounding environment. These out of equilibrium processes occur through cellular energy consumption, allowing biological systems to be described by active matter physics. Cytoskeleton filaments, bacterial and eukaryotic cells can be considered as a sub-class of active matter termed "active nematics". These biological objects can be modelled as rod-like elements to which nematic liquid crystal theories can be applied. In this work, using an analogy from liquid crystal physics, we show that cell sorting and boundary formation can be explained using differences in nematic activity. This difference in nematic activity arises from a balance of inter- and intra-cellular activity.

Highlights

  • Biological systems develop mechanical forces to perform their functions at molecular, cellular and tissue levels [1, 2] and their mechanical behaviour is largely controlled by components that are out of thermodynamic equilibrium

  • Biological systems like cytoskeleton filaments; bacteria or eukaryotic cellular assemblies can be described using an important sub-class of active systems that relies on their rod-like shape called active nematics

  • At long time and large length scales, isotropic structures can be seen as fluids or gels and long range orientational orders of these particles results in a liquid crystal (LC) phase

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Summary

Introduction

Biological systems develop mechanical forces to perform their functions at molecular, cellular and tissue levels [1, 2] and their mechanical behaviour is largely controlled by components that are out of thermodynamic equilibrium. One would assume these individual contractile cells to generate contractile stresses in a monolayer While this is true for a monolayer of fibroblasts [21], epithelial monolayers [13, 22] and a monolayer of neural progenitor cells [16] display extensile behaviour, that is the net force from the neighbours and substrate interaction acts to elongate the cell further along its long axis (Box 2). This poses a question on the emergence of extensile stresses within a collection of single contractile units and how this change in active behaviour of cells give rise to the tissue architecture observed in-vivo. Contractile stresses drive movement of +1/2 defect towards the tail direction (Figure B)

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