Principles of Actomyosin Regulation In Vivo

The actomyosin cytoskeleton is responsible for most force-driven processes in cells and tissues. How it assembles into the necessary structures at the right time and place is an important question. Here, we focus on molecular mechanisms of actomyosin regulation recently elucidated in animal models, and highlight several common principles that emerge. The architecture of the actomyosin network – an important determinant of its function – results from actin polymerization, crosslinking and turnover, localized myosin activation, and contractility-driven self-organization. Spatiotemporal regulation is achieved by tissue-specific expression and subcellular localization of Rho GTPase regulators. Subcellular anchor points of actomyosin structures control the outcome of their contraction, and molecular feedback mechanisms dictate whether they are transient, cyclic, or persistent. Actomyosin contractility, which shapes cells and tissues during development, wound repair, and physiology, is regulated by the actin network architecture, connectivity and turnover, as well as myosin-II dependent self-organization. Spatiotemporal regulation of contractility results from localized and timely activation of Rho signaling downstream of cellular polarity regulators, or membrane receptors and tissue-specific transcription factors. Anchoring of actomyosin structures at cell–cell and cell–extracellular matrix adhesions is important for force transmission, as well as regulation of contractility. Mechanical feedback from adhesions on actomyosin regulates developmental processes. Feedback loops generating cycles of Rho activation and inactivation are responsible for pulsatile contractile behaviors that are prevalent in animal development and physiology.