ABSTRACT
The description of cell migration by the action of a lamellipodium given in [15] is reproduced here for completeness. Cells migrate by protruding at the front and retracting at the rear. Protrusion occurs in thin membrane-bound cytoplasmic sheets, 0.2 to 0.3 m thick and several microns long, termed lamellipodia [22]. The major structural components of lamellipodia are actin filaments, which are organized in a more or less 2-D diagonal array with the fast-growing plus ends of the actin filaments directed forward, abutting the membrane [21]. Protrusion is effected by actin polymerization, whereby actin monomers are inserted at the plus ends of the filaments at the membrane interface and removed at the minus ends, throughout and at the base of the lamellipodium, in a treadmilling regime [16]. Stabilization of the actin meshwork is achieved by the crosslinking of the filaments by actin-associated proteins, such as filamin [12], as well as protein complexes such as the Arp2/3 [18], although the density and location of such crosslinks remain to be established. Because actin polymerization is involved in diverse motile processes aside from cell motility, including endocytosis and the propulsion of pathogens that invade cytoplasm [2], the question of how actin filaments are able to push against a membrane has spawned the development of various models [9].
