My research

Tissue fluidity depends on the ability to exchange cell neighbors. However, this process, known as T1 topological transition, has been oversimplified in existing models, leaving the cell mechanisms driving the formation of multicellular vertices (rosettes) and tissue fluidity poorly understood. Recent cell-level experiments, demonstrating increased tension in response to contraction, prompted us to explore tissue-level tension remodeling based on local strain. We developed a cell-based computational model incorporating a coarse-grained mechano-chemical feedback mechanism. We found that such feedback controls the fluid of the tissue, defining solid tissues when the remodeling rates are low, and fluid tissues when are high. Furthermore, for high enough remodeling induced by stretch,  multicellular vertices (rosettes) emerge, resembling those observed in living issues during early development.

Tissues often display pulsatory activity patterns, yet the underlying mechanisms and the contribution of cell-level properties remain elusive. Through numerical simulations and analytical calculation, we showed that  feedback between stretch and contractility is sufficient to explain the emergence of traveling waves and traveling pulse in confluent tissues. Our findings highlight that the transition from pulse to long-range wave propagation at multicellular scales is driven by the competition of cell-level mechanical response timescales, and geometrical disorder.

Before epiboly,  the epithelial tissue covering the annual killifish Austrolebias nigripinnis shows uncoordinated cell apical constriction pulses. Starting from the classical vertex model for confluent tissues, we investigate two cell activities causing cell area contraction: perimeter activity (a decrease in the preferred perimeter) and medial activity (a decrease in the preferred area). Interestingly, the dynamics of cell shape differ in each case. Using geometrical data from live embryo imaging, we predict that the tissue is undergoing medial relaxation, and the pulses are driven by perimeter activity.

The stability of tissues plays a crucial role in shaping organisms during early development. By using computational simulations and analytical methods, we've found that mechanical instabilities can arise due to internal cellular activity or external stresses. Specifically, when using the vertex model to describe these tissues computationally, the instability leads to cell elongation (at short times),  followed by the formation of non-convex polygons (at longer times), where the model ceases to be valid. Interestingly, we've discovered that in confluent tissues, shear modes of cell deformation are coupled to rotation and deviatoric modes. As a result, we find that a vanishing shear modulus doesn't necessarily indicate an unstable tissue state.