Cell migration--movin' on.

Abstract

Cell migration is crucial for embryonic development, the inflammatory immune response, wound repair, and tumor formation and metastasis (1). It begins with an initial protrusion or extension of the plasma membrane at the front (leading edge) of the cell (see the figure). The protrusions are driven by the polymerization of a network of cytoskeletal actin filaments and are stabilized through the formation of adhesive complexes. These adhesive complexes are regions of the plasma membrane where integrin receptors, actin filaments, and associated proteins cluster together. As the cells migrate, the small nascent adhesive complexes (focal complexes) at the front of the cell grow and strengthen into larger, more organized adhesive complexes (focal adhesions) that serve as points of traction over which the body of the cell moves. Finally, release of adhesions at the rear results in a net displacement of the cell. The mechanisms that regulate the formation of focal complexes at the cell's leading edge and the release of focal adhesions at the cell's rear remain unclear. Now, on page 1172 of this issue, Smilenov et al. (2) demonstrate that focal adhesions are highly motile in stationary fibroblasts yet stationary in migrating fibroblasts, suggesting the existence of a molecular clutch that couples traction and contractile forces. Other recent findings highlight the importance of tension, the actin and myosin filament network, the Rho/Rac family of signaling molecules, and microtubules in cell migration. Coordinating all of these complex processes is the challenge facing cells that are on the move.