Cell adhesion and motility depend strongly on the
interactions between cells and extracellular matrix
(ECM) substrates. When plated onto artificial adhesive
surfaces, cells first flatten and deform extensively
as they spread. At the molecular level, the interaction
of membrane-based integrins with the ECM has been
shown to initiate a complex cascade of signaling
events [1], which subsequently triggers cellular morphological changes and results in the generation of
contractile forces [2]. Here, we focus on the early
stages of cell spreading and probe their dynamics by
quantitative visualization and biochemical manipulation with a variety of cell types and adhesive surfaces,
adhesion receptors, and cytoskeleton-altering drugs.
We find that the dynamics of adhesion follows a universal power-law behavior. This is in sharp contrast with
the common belief that spreading is regulated by either
the diffusion of adhesion receptors toward the growing
adhesive patch [3–5] or by actin polymerization [6–8].
To explain this, we propose a simple quantitative and
predictive theory that models cells as viscous adhesive cortical shells enclosing a less viscous interior.
Thus, although cell spreading is driven by well-identified biomolecular interactions, it is dynamically limited
by its mesoscopic structure and material properties.