Cell Protrusions

Introduction How do cells move? There is no shortage of theories, but a definitive answer is still elusive. Here we will present some models for cell motions along with proposals for experiments to address the theories. We will restrict ourselves to the problem of cell protrusion, although the models apply to other motility phenomena as well. Different protrusion phenomena extend at different characteristic rates. Figure 1 shows data for protrusion rates of lamellipodia, filopodia and the acrosomal process of Thyone. Their velocities vary dramatically, which suggests that the force driving them may originate from different physical mechanisms. We will present here models for each of these processes. Lamellipodia are broad, flat cytoplasmic protrusions that spread out in front of a moving cell. Experiments have shown that there is surface flow of cytoplasm rearward from the leading edge as the lamellipodium extends forward [20]. Conservation of mass ensures that there must be a central flow of cytoplasm forward to provide the material for extension. The question we address is: what forces drive the extension of the leading lamella? Amoebae pseudopodia bear superficial resemblance to lamellipodia, but there is evidence that they may operate by a different mechanism, and so we will not deal with them here; models of the " frontal contraction " and " cortical tractor " hypotheses for amoeboid motion An elegant set of models have been developed by Dembo, Alt, and their coworkers based on the idea that cytoplasm can be modeled as a " contractile fluid " [1, 7, 8, 9]. They model the cytogel as a two-phase, viscous fluid (i.e. a Navier-Stokes system) with a term added that permits the gel phase to contract, then disassemble. Their numerical simulations show that such a fluid can indeed drive cytoplasmic flows in ways that appear realistic. Their model assumes the force driving the fluid phase derives from myosin-driven sliding of (counter-oriented) actin fibers and that neither cytoskeletal elasticity nor osmotic pressure play an important role. The contraction of the actin phase creates hydrostatic pressure gradients that impel the cytoplasm forward. While this model has much to recommend it, there are two experiments that cause some difficulty. First, scanning microscopy of the leading lamella reveals an apparently random, anastamosing network of actin fibers, rather than a fluid of shorter and/or counter-oriented filaments that could support myosin driven contraction [14, 15]. Second, opening fluid channels to the extracellular environment should …