Tissue models with active feecback*

Epithelial tissues are one of the engines of development in multicellular organism, where they determine the emerging shapes, like during the gastrulation process where the embryo turns inside out. This feat is performed by the active stresses generated by the cytoskeleton, where cells coordinate their collective mechanics over large spatial distances. In contrast to chemical signalling, we do not understand how surch coordinated activity or mechanical signalling work.

Here I will present models of vertex models of epithelial tissues with active feedback. In the early stages of gastrulation in the chick embryo, tissue deformation is driven by convergent-extension flows where tissue flows through active T1 transitions, against the applied stress, and actomyosin localises along pronounced myosin tension chains. We first develop a single junction active element where catch-bond dynamics of actomyosin allows the junction to work as an egine that can contract to a single point under applied stress. At the tissue scale, such elements coupled to a vertex model enable active T1 transitions, which occur in an optimal applied tension and activity range and each contribute a discrete negative strain amount, thus acting like element of an active metamaterial. In a full, disordered tissue, active T1 transitions occur along pronounced tension chain structures, with emergent convergent-extension flow, i.e. a negative shear modulus, in agreement with experiment. We find that states of self-stress dominate the mechanics this model tissue, with stress localisation that resembles mechanical spring networks. I will conclude with recent results that show that tension chains emerge generically in such tissue models, in a process mirorring the compressive force chains of granular packings.