In conclusion, our study discloses a consistent rheological trend induced by EMT in human cells of diverse tissue origin, reflecting major structural changes of the actin cytoskeleton upon EMT.Chemotactic migration of bacteria-their ability to direct multicellular motion along chemical gradients-is central to processes in agriculture, the environment, and medicine. However, current understanding of migration is based on studies performed in bulk liquid, despite the fact that many bacteria inhabit tight porous media such as soils, sediments, and biological gels. Here, we directly visualize the chemotactic migration of Escherichia coli populations in well-defined 3D porous media in the absence of any other imposed external forcing (e.g., flow). We find that pore-scale confinement is a strong regulator of migration. Strikingly, cells use a different primary mechanism to direct their motion in confinement than in bulk liquid. Furthermore, confinement markedly alters the dynamics and morphology of the migrating population-features that can be described by a continuum model, but only when standard motility parameters are substantially altered from their bulk liquid values to reflect the influence of pore-scale confinement. Our work thus provides a framework to predict and control the migration of bacteria, and active matter in general, in complex environments.Cell migration is astoundingly diverse. Molecular signatures, cell-cell interactions, and environmental structures each play their part in shaping cell motion, yielding numerous morphologies and migration modes. Nevertheless, in recent years, a simple unifying law was found to describe cell migration across many different cell types and contexts faster cells turn less frequently. This universal coupling between speed and persistence (UCSP) was explained by retrograde actin flow from front to back, but it remains unclear how this mechanism generalizes to cells with complex shapes and cells migrating in structured environments, which may not have a well-defined front-to-back orientation. Here, we present an in-depth characterization of an existing cellular Potts model, in which cells polarize dynamically from a combination of local actin dynamics (stimulating protrusions) and global membrane tension along the perimeter (inhibiting protrusions). We first show that the UCSP emerges spontaneously in this model through a cross talk of intracellular mechanisms, cell shape, and environmental constraints, resembling the dynamic nature of cell migration in vivo. Importantly, we find that local protrusion dynamics suffice to reproduce the UCSP-even in cases in which no clear global, front-to-back polarity exists. VX-661 mw We then harness the spatial nature of the cellular Potts model to show how cell shape dynamics limit both the speed and persistence a cell can reach and how a rigid environment such as the skin can restrict cell motility even further. Our results broaden the range of potential mechanisms underlying the speed-persistence coupling that has emerged as a fundamental property of migrating cells.Myopia is a common ocular disorder with significant alterations in the anterior ocular structure, including the cornea. The cell biophysical phenotype has been proposed to reflect the state of various diseases. However, the biophysical properties of corneal cells have not been characterized during myopia progression and their relationship with myopia remains unknown. This study characterizes the biophysical properties of corneal cells in normal, myopic, and recovered conditions, using two classical myopia models. Surprisingly, myopic corneal cells considerably reduce F-actin and microtubule content and cellular stiffness and generate elevated traction force compared with control cells. When myopia is restored to the healthy state, these biophysical properties are partially or fully restored to the levels of control cells. Furthermore, the level of chromatin condensation is significantly increased in the nucleus of myopic corneal cells and reduced to a level similar to healthy cells after recovery. These findings demonstrate that the reversible biophysical alterations of corneal cells reflect myopia progression, facilitating the study of the role of corneal cell biophysics in myopia.γ-Aminobutyric acid type A (GABAA) receptors in the brain are located in the outer membranes of brain cells where the concentration of cholesterol is high. Of the 25 available high-resolution structures available for GABAA receptors, none were determined in the presence of cholesterol, but four include resolved molecules of cholesterol hemisuccinate (CHS). Here, a molecular docking procedure is used to sweep the transmembrane (TM) surfaces of the receptors for cholesterol binding sites. Cholesterol docking poses determined in this way match 89% of the resolved CHS when CHS molecules deemed unlikely to represent typical bound cholesterols are excluded. The receptors are pentameric, and their TM surfaces consist of a set of five facets, each including pairs of TM helices from two adjacent subunits. Each facet contains hydrophobic hollows running from one side of the membrane to the other, within which are six potential binding sites for cholesterol, three on each side of the membrane. High-resolution structures of GABAA receptors with bound neurosteroids show that neurosteroids bind in these cholesterol binding sites, so the binding of neurosteroids and cholesterol will be competitive.Erk signaling regulates cellular decisions in many biological contexts. Recently, we have reported a series of Erk activity traveling waves that coordinate regeneration of osteoblast tissue in zebrafish scales. These waves originate from a central source region, propagate as expanding rings, and impart cell growth, thus controlling tissue morphogenesis. Here, we present a minimal reaction-diffusion model for Erk activity waves. The model considers three components Erk, a diffusible Erk activator, and an Erk inhibitor. Erk stimulates both its activator and inhibitor, forming a positive and negative feedback loop, respectively. Our model shows that this system can be excitable and propagate Erk activity waves. Waves originate from a pulsatile source which is modeled by adding a localized basal production of the activator, which turns the source region from an excitable to an oscillatory state. As Erk activity periodically rises in the source, it can trigger an excitable wave which travels across the entire tissue.