Cell adhesion is a paradigm of the ubiquitous interplay of cell signalling, modulation of material properties and biological functions of cells. It is controlled by competition of short range attractive forces, medium range repellant forces and the elastic stresses associated with local and global deformation of the composite cell envelopes. We review the basic physical rules governing the physics of cell adhesion learned by studying cell-mimetic systems and demonstrate the importance of these rules in the context of cellular systems. We review how adhesion induced micro-domains couple to the intracellular actin and microtubule networks allowing cells to generate strong forces with a minimum of attractive cell adhesion molecules (CAMs) and to manipulate other cells through filopodia over micrometer distances. The adhesion strength can be adapted to external force fluctuations within seconds by varying the density of attractive and repellant CAMs through exocytosis and endocytosis or protease-mediated dismantling of the CAM–cytoskeleton link. Adhesion domains form local end global biochemical reaction centres enabling the control of enzymes. Actin–microtubule crosstalk at adhesion foci facilitates the mechanical stabilization of polarized cell shapes. Axon growth in tissue is guided by attractive and repulsive clues controlled by antagonistic signalling pathways.

We present a systematic comparison of microrheological and macrorheological measurements of the viscoelastic storage and loss moduli, $G^{\prime }\mathrm{}\left(f\right)\mathrm{}$ and $G^{″}\mathrm{}\left(f\right),$ respectively, of solutions of the semiflexible biopolymer F-actin. Using magnetic tweezers microrheometry and rotating disk macrorheometry, we show that microscopic values for $G^{\prime }\mathrm{}\left(f\right)\mathrm{}$ and $G^{″}\mathrm{}\left(f\right)\mathrm{}$ are significantly smaller than macroscopic results over the frequency range $f=0.004\mathrm{}–4$ Hz, whereas the qualitative shape of the spectra is similar. These findings confirm recent theoretical predictions [A. C. Maggs, Phys. Rev. E 57, 2091 (1998)]. The discrepancy affects not only absolute values of $G^{\prime }\mathrm{}\left(f\right)\mathrm{}$ and $G^{″}\mathrm{}\left(f\right):$ although microscopic and macroscopic plateau regime are found in the same frequency range, the two methods yield different values for the entanglement time which determines the high-frequency end of the plateau. By investigating F-actin solutions of different mean filament lengths, we show that microscopic and macroscopic $G^{\prime }\mathrm{}\left(f\right)\mathrm{}$ and $G^{″}\mathrm{}\left(f\right)\mathrm{}$ converge, if the probe particle used in microrheometry becomes large compared to the length of actin filaments.

The survival of cells depends on perpetual active motions, including (a) bending excitations of the soft cell envelopes, (b) the bidirectional transport of materials and organelles between the cell center and the periphery, and (c) the ongoing restructuring of the intracellular macromolecular scaffolds mediating global cell changes associated with cell adhesion locomotion and phagocytosis. Central questions addressed are the following: How can this bustling motion of extremely complex soft structures be characterized and measured? What are the major driving forces? Further topics include (a) the active dynamic control of global shape changes by the interactive coupling of the aster-like soft scaffold of microtubules and the network of actin filaments associated with the cell envelope (the actin cortex) and (b) the generation of propulsion forces by solitary actin gelation waves propagating within the actin cortex.