Abstract
Tissue remodeling requires cell shape changes associated with pulsation and flow of the actomyosin cytoskeleton. Here we describe the hydrodynamics of actomyosin as a confined active elastomer with turnover of its components. Our treatment is adapted to describe the diversity of contractile dynamical regimes observed in vivo. When myosin-induced contractile stresses are low, the deformations of the active elastomer are affine and exhibit spontaneous oscillations, propagating waves, contractile collapse and spatiotemporal chaos. We study the nucleation, growth and coalescence of actomyosin-dense regions that, beyond a threshold, spontaneously move as a spatially localized traveling front. Large myosin-induced contractile stresses lead to nonaffine deformations due to enhanced actin and crosslinker turnover. This results in a transient actin network that is constantly remodeling and naturally accommodates intranetwork flows of the actomyosin-dense regions. We verify many predictions of our study in Drosophila embryonic epithelial cells undergoing neighbor exchange during germband extension.
Highlights
Tissue remodeling requires cell shape changes associated with pulsation and flow of the actomyosin cytoskeleton
We model the medial actomyosin mesh as an active elastomer embedded in a solvent, subject to active contractile stresses arising from the binding of myosin minifilaments (Fig. 1a)[5, 7, 15, 16], and turnover of all components
We model the medial actomyosin crosslinked mesh as an active elastomer embedded in a solvent, subject to active contractile stresses arising from the binding of myosin minifilaments (Fig. 1a)[5, 7, 15, 16], and turnover of all components
Summary
Tissue remodeling requires cell shape changes associated with pulsation and flow of the actomyosin cytoskeleton. Large myosin-induced contractile stresses lead to nonaffine deformations due to enhanced actin and crosslinker turnover This results in a transient actin network that is constantly remodeling and naturally accommodates intranetwork flows of the actomyosin-dense regions. Large myosin-induced contractile stresses can lead to nonaffine deformations due to actin turnover or network rupture This results in a transient actin network that exhibits large intermittent strain fluctuations and intranetwork flow of the actomyosin-dense regions as a consequence of filament unbinding and rebinding. Both the affine and nonaffine theories predict that the driving force for spontaneous movement comes from the actomyosin-dense region itself and not the cell boundary—we provide robust experimental verification of this. Our general perspective reveals several significantly new aspects and provides a fresh conceptual understanding of this ubiquitous phenomenon
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