Abstract

It has long been established that biological tissues are viscoelastic materials, and that embryonic tissues in particular have an ability to flow over large distances on long time scales. The mechanical properties of these tissues likely play an important role in cell movements and pattern formation during embryogenesis, cancer and regeneration, and they can be measured using rheology techniques such as tissue surface tensiometry (TST).Over the past 40 years, two theories have been advanced to explain the microscopic origins of tissue surface tension: the differential adhesion hypothesis (DAH) and the differential interfacial tension hypothesis (DITH). While the DAH contributes surface tension to adhesive energies, the DITH contributes it purely to cortex tensions. The DAH has been able to successfully explain a vast range of data on embryonic and cancer cell aggregates and tissues over the last decades, however, recent studies on single cells appear to support the DITH.Here we show that a simple mechanical model which accounts for cell-cell adhesion, cortical tension, and fluid incompressibility can explain the two types of experimental data within a single framework. We find that tissue surface tension is a careful balance between adhesive and tensile forces, which are interdependent and cannot be altered independently; the relative strength of adhesive and tensile forces determines the measured macroscopic surface tension.In addition, the model predicts that cells on the surface of an aggregate alter their morphology as the surface tension changes, and we will present experimental data from embryonic tissues that are consistent with these predictions.

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