The intrinsic genetic program of a cell is not sufficient to explain all of the cell’s activities. External mechanical stimuli are increasingly recognized as determinants of cell behavior. In the epithelial folding event that constitutes the beginning of gastrulation in Drosophila, the genetic program of the future mesoderm leads to the establishment of a contractile actomyosin network that triggers apical constriction of cells and thereby tissue folding. However, some cells do not constrict but instead stretch, even though they share the same genetic program as their constricting neighbors. We show here that tissue-wide interactions force these cells to expand even when an otherwise sufficient amount of apical, active actomyosin is present. Models based on contractile forces and linear stress–strain responses do not reproduce experimental observations, but simulations in which cells behave as ductile materials with nonlinear mechanical properties do. Our models show that this behavior is a general emergent property of actomyosin networks in a supracellular context, in accordance with our experimental observations of actin reorganization within stretching cells.
The intrinsic genetic programme of a cell is not always sufficient to explain the cell's activities. External mechanical stimuli are increasingly recognized as determinants of cell behaviour. In the epithelial folding event that constitutes the beginning of gastrulation in Drosophila, the genetic programme of the future mesoderm leads to the establishment of a contractile actomyosin network that triggers apical constriction of cells, and thereby, furrow formation. However, some cells do not constrict but instead stretch, even though they share the same genetic programme as their constricting neighbours. We show here that tissue-wide interactions force a subset of cells to expand even when an otherwise sufficient amount of apical, active actomyosin is present. Models based on contractile forces and linear-stress strain responses are not sufficient to reproduce experimental observations, but simulations in which cells behave as ductile materials with non-linear mechanical properties do. Our models show that this behaviour is an emergent property of supracellular actomyosin networks, in accordance with our experimental observations of actin reorganization within stretching cells.
The intrinsic genetic programme of a cell is not always sufficient to explain the cell's activities. External mechanical stimuli are increasingly being recognized as determinants of cell behavior. In the epithelial folding event that constitutes the beginning of gastrulation in Drosophila, the genetic programme of the future mesoderm leads to the establishment of a contractile actomyosin network that triggers apical constriction of cells, and thereby, furrow formation. However, some cells do not constrict but instead stretch, even though they share the same genetic programme as their constricting neighbors. We show here that tissue-wide interactions override the intrinsic programme of a subset of cells, forcing them to expand even when an otherwise sufficient amount and concentration of apical, active actomyosin has been accumulated. Models based on contractile forces and linear stress-strain responses are not sufficient to reproduce experimental observations, but simulations in which cells behave as materials with non-linear mechanical properties do. Our models also show that this behavior is an emergent property of supracellular actomyosin networks, in accordance with our experimental observations of actin reorganization within streching cells, with this event being stochastic and rare in cells with high myosin levels, but reproducible in cells with lower concentrations.
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