A magnetic bead microrheometer has been designed which allows the generation of forces up to 10(4) pN on 4.5 micron paramagnetic beads. It is applied to measure local viscoelastic properties of the surface of adhering fibroblasts. Creep response and relaxation curves evoked by tangential force pulses of 500-2500 pN (and approximately 1 s duration) on the magnetic beads fixed to the integrin receptors of the cell membrane are recorded by particle tracking. Linear three-phasic creep responses consisting of an elastic deflection, a stress relaxation, and a viscous flow are established. The viscoelastic response curves are analyzed in terms of a series arrangement of a dashpot and a Voigt body, which allows characterization of the viscoelastic behavior of the adhering cell surface in terms of three parameters: an effective elastic constant, a viscosity, and a relaxation time. The displacement field generated by the local tangential forces on the cell surface is visualized by observing the induced motion of assemblies of nonmagnetic colloidal probes fixed to the membrane. It is found that the displacement field decays rapidly with the distance from the magnetic bead. A cutoff radius of Rc approximately 7 micron of the screened elastic field is established. Partial penetration of the shear field into the cytoplasm is established by observing the induced deflection of intracellular compartments. The cell membrane was modeled as a thin elastic plate of shear modulus mu * coupled to a viscoelastic layer, which is fixed to a solid support on the opposite side; the former accounts for the membrane/actin cortex, and the latter for the contribution of the cytoskeleton to the deformation of the cell envelope. It is characterized by the coupling constant chi characterizing the elasticity of the cytoskeleton. The coupling constant chi and the surface shear modulus mu * are obtained from the measured displacements of the magnetic and nonmagnetic beads. By analyzing the experimental data in terms of this model a surface shear modulus of mu * approximately 2 . 10(-3) Pa m to 4 . 10(-3) Pa m is found. By assuming an approximate plate thickness of 0.1 micron one estimates an average bulk shear modulus of mu approximately (2 / 4) . 10(-4) Pa, which is in reasonable agreement with data obtained by atomic force microscopy. The viscosity of the dashpot is related to the apparent viscosity of the cytoplasm, which is obtained by assuming that the top membrane is coupled to the bottom (fixed) membrane by a viscous medium. By application of the theory of diffusion of membrane proteins in supported membranes we find a coefficient of friction of bc approximately 2 . 10(9) Pa s/m corresponding to a cytoplasmic viscosity of 2 . 10(3) Pa s.

We report a study of the deformability of a bacterial wall with an atomic force microscope (AFM). A theoretical expression is derived for the force exerted by the wall on the cantilever as a function of the depths of indentation generated by the AFM tip. Evidence is provided that this reaction force is a measure for the turgor pressure of the bacterium. The method was applied to magnetotactic bacteria of the species Magnetospirillum gryphiswaldense. Force curves were generated on the substrate and on the bacteria while scanning laterally. With the mechanical properties so gained we obtained the spring constant of the bacterium as a whole. Making use of our theoretical results we determined the turgor pressure to be in the range of 85 to 150 kPa.

We report the first measurement of the kinetics of adhesion of a single giant vesicle controlled by the competition between membrane-substrate interaction mediated by ligand-receptor interaction, gravitation, and Helfrich repulsion. To model the cell-tissue interaction, we doped the vesicles with lipid-coupled polymers (mimicking the glycocalix) and the reconstituted ligands selectively recognized by alpha(IIb)beta(3) integrin-mediating specific attraction forces. The integrin was grafted on glass substrates to act as a target cell. The adhesion of the vesicle membrane to the integrin-covered surface starts with the spontaneous formation of a small (approximately 200 nm) domain of tight adhesion, which then gradually grows until the whole adhesion area is in the state of tight adhesion. The time of adhesion varies from few tens of seconds to about one hour depending on the ligand and lipopolymer concentration. At small ligand concentrations, we observed the displacement xi of the front of tight adhesion following the square root law xi approximately t(1/2), whereas, at high concentrations, we found a linear law xi approximately t. We show both experimentally and theoretically that the t(1/2)-regime is dominated by diffusion of ligands, and the xi approximately t-regime by the kinetics of ligands-receptors association.

We used micropipettes to aspirate leading and trailing edges of wild-type and mutant cells of Dictyostelium discoideum. Mutants were lacking either myosin II or talin, or both proteins simultaneously. Talin is a plasma membrane-associated protein important for the coupling between membrane and actin cortex, whereas myosin II is a cytoplasmic motor protein essential for the locomotion of Dictyostelium cells. Aspiration into the pipette occurred above a threshold pressure only. For all cells containing talin this threshold was significantly lower at the leading edge of an advancing cell as compared to its rear end, whereas we found no such difference in cells lacking talin. Wild-type and talin-deficient cells were able to retract from the pipette against an applied suction pressure. In these cells, retraction was preceded by an accumulation of myosin II in the tip of the aspirated cell lobe. Mutants lacking myosin II could not retract, even if the suction pressures were removed after aspiration. We interpreted the initial instability and the subsequent plastic deformation of the cell surface during aspiration in terms of a fracture between the cell plasma membrane and the cell body, which may involve destruction of part of the cortex. Models are presented that characterize the coupling strength between membrane and cell body by a surface energy sigma. We find sigma approximately 0.6(1.6) mJ/m(2) at the leading (trailing) edge of wild-type cells.

We establish a model of cell-tissue interaction consisting of vesicles carrying lipopolymers (to mimic the glycocalix) and mobile specific ligands of the blood platelet integrin α IIb β3 covering the substrate. We find the phase diagram with a first-order transition between a gravity-controlled weak state of the vesicle-substrate adhesion and a strong-adhesion state governed by receptor-ligand interaction. Adhesion energy ε adh is measured as a function of ligand and repeller concentration by interferometric contour analysis on the basis of a new refined model of soft shell adhesion (accounting for the membrane bending and stretching at the adhesion rim of the ellipsoidal vesicle). At ligand densities comparable to integrin density, ε adh decreases sharply. Increasing the repeller content weakens the adhesion strength.

In studying a magnetic bead's creep response to force pulses in an entangled actin network we have found a novel regime where the bead motion obeys a power law x(t) approximately t(1/2) over two decades in time. It is flanked by a short-time regime with x(t) approximately t(3/4) and a viscous with x(t)approximately t. In the intermediate regime the creep compliance depends on the actin concentration c as c(-beta) with beta approximately 1.1 +/- 0.3. We explain this behavior in terms of osmotic restoring force generated by the piling up of filaments in front of the moving bead. A model based on this concept predicts intermediate x(t) approximately t(1/2) and long-time regimes x(t) approximately t in which the compliance varies as c(-4/3), in agreement with experiment.

We report a theoretical calculation of the elasticity of the peptidoglycan network, the only stress-bearing part of rod-shaped Gram-negative eubacteria. The peptidoglycan network consists of elastic peptides and inextensible glycan strands, and it has been proposed that the latter form zigzag filaments along the circumference of the cylindrical bacterial shell. The zigzag geometry of the glycan strands gives rise to nonlinear elastic behavior. The four elastic moduli of the peptidoglycan network depend on its stressed state. For a bacterium under physiological conditions the elasticity is proportional to the bacterial turgor pressure. Our results are in good agreement with recent measurements.

General properties of nucleation of elastic defects in crystals undergoing a phase transition are described in the framework of a Landau-type approach. For static defects the phase diagram topology of a nucleus is shown to be independent of the nature and geometry of the defects and may contain additional phases which are unstable in the bulk. For moving defects the nuclei have a specific configuration and arise only below a critical speed of the defects. [S0031-9007 (98)06687-3] PACS numbers: 64.60.Qb, 81.30. -t, 81.40.Np, 82.60.Nh Elastic defects such as dislocations, cracks, inclusions, or twin boundaries often give rise, in the vicinity of a phase transition, to nuclei of a new phase close to the defects [1-8]. These nuclei have been observed in many categories of transitions and materials, i.e., in martensitic-type transformations in metals and alloys [1], in ceramics [2], in magnetic [3] and ferroelectric or ferroelastic transitions [4,5], in Mott transitions [6], in semicrystalline polymers [7], as well as in superconducting materials [8].In contrast to the unstable Frenkel nuclei which are due to thermal fluctuations [9], nuclei associated with elastic defects are stabilized by the strain field induced by the defects. This fact was first recognized by Cahn [10], who proposed thermodynamic model of nucleation in the case of dislocations. Further theoretical approaches [11] described nucleation for specific elastic defects and geometries. There exists, however, a number of general static and dynamic properties, which are common to the nucleation processes and are independent from the nature and geometry of the defects. The aim of this Letter is to describe these properties in a unified way, in the framework of a Landau-type approach [12]. More precisely, we will demonstrate successively the following: (i) The phase diagram topology of the nuclei is independent from the nature and geometry of the defects. (ii) In the vicinity of a multiphase point the structure of the nucleus may correspond to a symmetry which cannot be obtained in the bulk. (iii) The nucleation does not occur above a critical speed of the defects. (iv) Nuclei at moving defects display a specific configuration.Let us first consider a crystal undergoing a phase transition taking place at T c , associated with a one-component order parameter h. The Landau-Ginsburg free energy of a crystal involving elastic defects can be expressed under the general form,