Fig. 11 Models of cell body translocation. Actin filaments are shown as grey lines, and myosin filaments, as black lines or dumbbell figures. (I) The sarcomeric mechanism cannot drive cell body forward because arc-shaped actin-myosin II bundles, upon contraction, would produce a backward directed net force on the cell body. (II) The transport model does not fit the data because myosin clusters in the lamellipodia, the only part of a cell where transport tracks are present, do not move forward. (III) Forward rolling driven by actin-myosin axles seems problematic because of the predominantly backward orientation of flanking bundles (a, top view). These bundles may participate in rolling by exerting a rearward directed force at the bottom (b, vertical section, however, the origin of forward directed force remains unclear (question mark). (IV) According to the dynamic network model, contraction of an actin-myosin network in the lamellipodia/cell body transition zone is coupled to forward translocation. (a) In the lamellipodium, the network of divergent actin filaments interacts with clusters of myosin bipolar filaments. Whereas small myosin clusters situated in the dense network close to cell front cannot move, bigger clusters in the sparser network in the transition zone are capable of approaching barbed ends of diverging filaments and moving forward. (b) As myosin clusters move forward, they align actin filaments parallel to the leading edge. (c) Overall, network contraction at the lamellipodia/cell body transition zone results in formation of actin-myosin bundles and forward translocation of the cell body. (d) Vertical section view shows that forward rolling would result from a combination of network contraction in front of the cell body with rearward drag resulting from actin-myosin bundles at the bottom of the body.