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Cells maintain a dynamic actin cytoskeleton by carefully balancing the activities of a diverse collection of actin regulators. Recent findings suggest that key actin assembly factors limit one another through competition over a finite pool of G-actin. Increasing or decreasing cellular G-actin influences the type of F-actin network generated. The actin monomer binding protein profilin is responsible for proportioning how much G-actin is available to each assembly factor. Cytoskeletal competition appears universally conserved from yeast to human. Competition ensures cytoskeletal homeostasis and integration/coordination between the different actin regulatory pathways to support dynamic cell behaviour. Dynamic rearrangements in the actin cytoskeleton underlie a wide range of cell behaviours, which in turn contribute to many aspects of human health including embryogenesis, cancer metastasis, wound healing, and inflammation. Precise control of the actin cytoskeleton requires the coordinated activity of a diverse set of different actin regulators. However, our current understanding of the actin cytoskeleton has focused on how individual actin regulatory pathways function in isolation from one another. Recently, competition has emerged as a means by which different actin assembly factors can influence each other's activity at the cellular level. Here such findings will be used to explore the possibility that competition within the actin cytoskeleton confers cellular plasticity and the ability to prioritise multiple conflicting stimuli. Dynamic rearrangements in the actin cytoskeleton underlie a wide range of cell behaviours, which in turn contribute to many aspects of human health including embryogenesis, cancer metastasis, wound healing, and inflammation. Precise control of the actin cytoskeleton requires the coordinated activity of a diverse set of different actin regulators. However, our current understanding of the actin cytoskeleton has focused on how individual actin regulatory pathways function in isolation from one another. Recently, competition has emerged as a means by which different actin assembly factors can influence each other's activity at the cellular level. Here such findings will be used to explore the possibility that competition within the actin cytoskeleton confers cellular plasticity and the ability to prioritise multiple conflicting stimuli.
Davidson et al. (Sat,) studied this question.
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