Analogies with inert soft condensed matter--such as viscoelastic liquids, pastes, foams, emulsions, colloids, and polymers--can be used to investigate the mechanical response of soft biological tissues to forces. A variety of experimental techniques and biophysical models have exploited these analogies allowing the quantitative characterization of the mechanical properties of model tissues, such as surface tension, elasticity, and viscosity. The framework of soft matter has been successful in explaining a number of dynamical tissue behaviors observed in physiology and development, such as cell sorting, tissue spreading, or the escape of individual cells from a tumor. However, living tissues also exhibit active responses, such as rigidity sensing or cell pulsation, that are absent in inert soft materials. The soft matter models reviewed here have provided valuable insight in understanding morphogenesis and cancer invasion and have set bases for using tissue engineering within medicine.

RhoA-inhibitory bacterial toxins, such as Staphylococcus aureus EDIN toxin, induce large transendothelial cell macroaperture (TEM) tunnels that rupture the host endothelium barrier and promote bacterial dissemination. Host cells repair these tunnels by extending actin-rich membrane waves from the TEM edges. We reveal that cyclic-AMP signaling produced by Bacillus anthracis edema toxin (ET) also induces TEM formation, which correlates with increased vascular permeability. We show that ET-induced TEM formation resembles liquid dewetting, a physical process of nucleation and growth of holes within a thin liquid film. We also identify the cellular mechanisms of tunnel closure and reveal that the I-BAR domain protein Missing in Metastasis (MIM) senses de novo membrane curvature generated by the TEM, accumulates at the TEM edge, and triggers Arp2/3-dependent actin polymerization, which induces actin-rich membrane waves that close the TEM. Thus, the balance between ET-induced TEM formation and resealing likely determines the integrity of the host endothelium barrier.