Abstract
Cell division and death can be regulated by the mechanical forces within a tissue. We study the consequences for the stability and roughness of a propagating interface by analyzing a model of mechanically regulated tissue growth in the regime of small driving forces. For an interface driven by homeostatic pressure imbalance or leader-cell motility, long and intermediate-wavelength instabilities arise, depending, respectively, on an effective viscosity of cell number change, and on substrate friction. A further mechanism depends on the strength of directed motility forces acting in the bulk. We analyze the fluctuations of a stable interface subjected to cell-level stochasticity, and find that mechanical feedback can help preserve reproducibility at the tissue scale. Our results elucidate mechanisms that could be important for orderly interface motion in developing tissues.
Highlights
Cell division and death can be regulated by the mechanical forces within a tissue
Ref. [32] calculated the steady-state surface fluctuations of a non-growing tissue maintained in its homeostatic state. In tissue replacement, such as in the developing Drosophila abdominal epidermis [33, 34], interface propagation occurs. This may be driven by imbalances in pressure associated with cell division, and/or directed cell motility, which cause the expansion of one tissue at the other’s expense
If cell number change is sensitive to mechanical forces [11, 35,36,37,38,39,40,41,42,43,44] it leads to a “homeostatic pressure” [8, 45,46,47] which can drive interface propagation without coherently-directed cell motility forces
Summary
Cell division and death can be regulated by the mechanical forces within a tissue. We study the consequences for the stability and roughness of a propagating interface, by analysing a model of mechanically-regulated tissue growth in the regime of small driving forces. If cell number change is sensitive to mechanical forces [11, 35,36,37,38,39,40,41,42,43,44] it leads to a “homeostatic pressure” [8, 45,46,47] which can drive interface propagation without coherently-directed cell motility forces. We study a model of competing epithelial tissues, with an interface driven by homeostatic pressure or by directed motility, acting either at the interface (a “leader-cell” limit) or in bulk [50] [51,52,53].
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