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Living cells adapt and respond actively to the mechanical properties of their environment. In addition to biochemical mechanotransduction, evidence exists for a myosin-dependent purely mechanical sensitivity to the stiffness of the surroundings at the scale of the whole cell. Using a minimal model of the dynamics of actomyosin cortex, we show that the interplay of myosin power strokes with the rapidly remodeling actin network results in a regulation of force and cell shape that adapts to the stiffness of the environment. Instantaneous changes of the environment stiffness are found to trigger an intrinsic mechanical response of the actomyosin cortex. Cortical retrograde flow resulting from actin polymerization at the edges is shown to bemodulated by the stress resulting from myosin contractility, which in turn, regulates the cell length in a force-dependent manner. The model describes the maximum force that cells can exert and the maximum speed at which they can contract, which are measured experimentally. These limiting cases are found to be associated with energy dissipation phenomena, which are of the same nature as those taking place during the contraction of a whole muscle. This similarity explains the fact that single non-muscle cell and whole-muscle contraction both follow a Hill-like force-velocity relationship. [ABSTRACT FROM AUTHOR]

Many cell movements proceed via a crawling mechanism, where polymerization of the cytoskeletal protein actin pushes out the leading edge membrane. In this model, membrane tension has been seen as an impediment to filament growth and cell motility. Here we use a simple model of cell motility, the Caenorhabditis elegans sperm cell, to test how membrane tension affects movement and cytoskeleton dynamics. To enable these analyses, we create transgenic worm strains carrying sperm with a fluorescently labeled cytoskeleton. Via osmotic shock and deoxycholate treatments, we relax or tense the cell membrane and quantify apparent membrane tension changes by the membrane tether technique. Surprisingly, we find that membrane tension reduction is correlated with a decrease in cell displacement speed, whereas an increase in membrane tension enhances motility. We further demonstrate that apparent polymerization rates follow the same trends. We observe that membrane tension reduction leads to an unorganized, rough lamellipodium, composed of short filaments angled away from the direction of movement. On the other hand, an increase in tension reduces lateral membrane protrusions in the lamellipodium, and filaments are longer and more oriented toward the direction of movement. Overall we propose that membrane tension optimizes motility by streamlining polymerization in the direction of movement, thus adding a layer of complexity to our current understanding of how membrane tension enters into the motility equation. [ABSTRACT FROM AUTHOR]

Many cells crawl by extending an actin-rich pseudopod. We have devised a simulation that describes how the polymerization kinetics of a branched actin filament network, coupled with excluded volume effects, powers the motility of crawling cells such as amoebae and fish keratocytes. Our stochastic simulation is based on the key fundamental properties of actin polymerization, namely growth, shrinkage, capping, branching, and nucleation, and also includes contributions from the creation and breaking of adhesive contacts with the substrate together with excluded volume effects related to filament packing. When reasonable values for appropriate constants were employed, this simulation generated a force-velocity relationship that resembled closely that observed experimentally. Our simulations indicated that excluded volume effects associated with actin filament branching lead to a decreased packing efficiency and resultant swelling of the cytoskeleton gel that contributes substantially to lamellipod protrusion. [ABSTRACT FROM AUTHOR]