We develop an analytical theory to explain the experimentally observed morphological transitions of quasispherical giant vesicles induced by alternating electric fields. The model treats the inner and suspending media as lossy dielectrics, and the membrane as an impermeable flexible incompressible-fluid sheet. The vesicle shape is obtained by balancing electric, hydrodynamic, bending, and tension stresses exerted on the membrane. Our approach, which is based on force balance, also allows us to describe the time evolution of the vesicle deformation, in contrast to earlier works based on energy minimization, which are able to predict only stationary shapes. Our theoretical predictions for vesicle deformation are consistent with experiment. If the inner fluid is more conducting than the suspending medium, the vesicle always adopts a prolate shape. In the opposite case, the vesicle undergoes a transition from a prolate to oblate ellipsoid at a critical frequency, which the theory identifies with the inverse membrane charging time. At frequencies higher than the inverse Maxwell-Wagner polarization time, the electrohydrodynamic stresses become too small to alter the vesicle's quasispherical rest shape. The model can be used to rationalize the transient and steady deformation of biological cells in electric fields.

The stability of spherical vesicles in alternating (ac) electric fields is studied theoretically for asymmetric conductivity conditions across their membranes. The vesicle deformation is obtained from a balance between the curvature elastic energies and the work done by the Maxwell stresses. The present theory describes and clarifies the mechanisms for the four types of morphological transitions observed experimentally on vesicles exposed to ac fields in the frequency range from 500 to 2 × 107 Hz. The displacement currents across the membranes redirect the electric fields toward the membrane normal to accumulate electric charges by the Maxwell−Wagner mechanism. These accumulated electric charges provide the underlying molecular mechanism for the morphological transitions of vesicles as observed on the micrometer scale.

The binding properties of biomolecules play a crucial role in many biological phenomena, especially cell adhesion. Whereas the attachment kinetics of soluble proteins is considered well known, complex behavior arises when protein molecules are bound to the cell membrane. We probe the hidden kinetics of ligand-receptor bond formation using single-molecule flow chamber assays and Brownian dynamics simulations. We show that, consistent with our recently proposed hypothesis, association requires a minimum duration of contact between the reactive species. In our experiments, ICAM-1 anchored on a flat substrate binds to anti-ICAM-1 coated onto flowing microbeads. The interaction potential between bead and substrate is measured by microinterferometry and is used as an ingredient to simulate bead movement. Our simulation calculates the duration of ligand-receptor contacts imposed by the bead movement. We quantitatively predict the reduction of adhesion probability measured for shorter tether length of the ligand or if a repulsive hyaluronan layer is added onto the surface. To account for our results, we propose that bond formation may occur in our system by crossing of a diffusive plateau in the energy landscape, on the timescale of 5 ms and an energy barrier of 5 k(B)T, before reaching the first detectable bound state. Our results show how to relate cell-scale behavior to the combined information of molecular reactivity and biomolecule submicron-scale environment.