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  • Abstract: Roles of Actomyosin Contractility in Force Generation and Cell Shape Changes, Y2
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Living cells need to generate mechanical forces to perform their physiological functions. The ability of cells to generate forces originates primarily from a non-equilibrium biopolymer network called the actin cytoskeleton. Myosin motor proteins walk on actin filaments (F-actin) in the actin cytoskeleton by consuming chemical energy stored in ATP, which results in tensile forces. This actomyosin contractility is responsible for force generation in both muscle and non-muscle cells. While it is well understood how muscle cells generate contractile forces, it still remains elusive how interactions between F-actin and myosin motors lead to force generation in non-muscle cells because unlike muscle cells, the actin cytoskeleton of non-muscle cells has a highly disorganized structure and consists of dynamic F-actin which turns over very rapidly. Force generated from the actomyosin contractility in non-muscle cells gives rise to a wide variety of interesting biomechanical phenomena. Due to its fundamental importance, the actomyosin contractility has been an active field of studies for decades. However, due to experimental limitations, it is very challenging to elucidate how forces from the actomyosin contractility facilitate the biomechanical phenomena by experiments alone. Computational models can help illuminate the intrinsic mechanisms by predicting and interpreting experimental results and by perturbing the system in ways that experiments cannot employ. We propose computational models to illuminate how forces are generated from actomyosin contractility and lead to the non-equilibrium behaviors in disorganized actin cytoskeleton.

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