LAMELLIPODIAL AND AMOEBOID CELL LOCOMOTION: THE ROLE OF ACTIN-CYCLING AND BLEB FORMATION
Cell migration depends on the rapid changes of the organization of actin filaments and generation of force by motor proteins. Vertebrate cells use two different mechanisms: mesenchymal or amoeboid migration. Cells migrating in mesenchymal mode are elongated and move over a two-dimensional substratum. They extend thin veil-like extensions at their leading face — lamellipodia, whose protrusion depend on polymerization and depolymerization processes of actin. During mesenchymal migration actin filaments are firmly connected by integrins to the extracellular matrix (ECM) at focal contacts, which serve as points of fixation for subsequent cell body traction by force producing actomyosin interactions. Cells migrating in amoeboid fashion are rounded and move through a three-dimensional ECM-network undergoing considerable shape changes and generating vesicle-like surface extensions — so-called blebs. These blebs and the migrating cells exhibit no or strongly reduced affinity to the ECM. Bleb formation depends on a transient decrease of plasma membrane stiffness and locally increased hydrostatic pressure, which is generated by actin-myosin interactions. Formation of numerous surface blebs is also typical of cells that undergo apoptotic cell death. Since these share a number of properties to blebs of amoeboid cells, an analysis is given of the distribution of some cytoskeletal components in apoptotic blebs.