| Summary: | Dramatic changes in tissue architecture can be produced by the cumulative action of individual cell movements within epithelia. During rapid developmental processes polarised recruitment of Myosin-II has previously been shown to drive changes in cell shape and direct neighbour exchange. It is important to ask whether similar mechanisms facilitate junction movement in stable epithelia, that are more prevalent in nature, and whether seemingly noisy fluctuations in junction length contribute to homeostatic tissue packing under ordinary growth conditions. By using the Drosophila notum, I have taken advantage of a model system that remains constant in overall size and shape, whilst it orders, as a result of changes in cells packing. Confocal live imaging enabled quantitative junction fluctuation measurements of control and RNAi expressing nota, before and after periods of cell division, delamination and bristle cell differentiation. Through a reduction in Myosin II (Myo II) activity, I established that junctional actomyosin was not required to drive neighbour exchange events in this tissue. Conversely, an increase in active Myo II levels was sufficient to inhibit junction fluctuations, cell intercalation and midline live cell delamination events. These results suggest a model in which Myo II independent junction length fluctuations fluidize the tissue, thereby enabling cells to move in order to relieve tissue stresses and crowding. Furthermore, over the course of pupal development a systematic re-localisation of medioapical actomyosin to the junction correlated with a rise in line tension and an increase in tissue order. Thus, changes to actomyosin levels appear to tune neighbour exchange in a process akin to annealing, as the tissue moves from a state of disorder to hexagonal packing prior to the completion of development.
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