Mechanisms of Protrusion and Cell Locomotion. Actomyosin-based Contraction in the Cell Body and Uropod Rather than Actin-based Motors at the Leading Front Drives Locomotion of Walker Carcinosarcoma Cells.

Abstract

Earlier models explaining cell locomotion are briefly reviewed. Then, a model explaining locomotion of non-adhesive Walker carcinosarcoma cells is proposed based on the following data: 1) Walker carcinosarcoma cells, which normally form lamellipodia, can produce forces for movement by at least two distinct actin-based mechanisms, 2) Lamellipodial motility is driven by local actin polymerization, but lamellipodia and actin-based mechanisms (polymerization or contraction) at the front are redundant for locomotion, 3) actomyosin-dependent contraction at the rear (body and/or uropod) is sufficient and necessary for locomotion, 4) fluid pressure can generate protrusion (blebs), 5) an intact cortical layer at the front tends to reduce the speed of locomotion, 6) there is no biologically significant difference in the efficiency of locomotion (speed, persistence, net displacement) of migrating cells showing either lamellipodia, blebs or no morphologically recognizable protrusions, 7) polymerized actin is concentrated in the cortical actin layer. Myosin IIA is preferentially associated with the actin cortex at the rear part of the cell. The data suggest that actomyosin-based contraction in the form of cortical contraction generates protrusion and locomotion in Walker carcinosarcoma cells as previously described in Amoebae. The role of actomyosin-dependent contraction and of fluid-driven mechanisms in other metazoan tissue cell lines is discussed.