Abstract
In order to understand how tissue mechanics shapes animal body, it is critical to clarify how cells respond to and resist tissue stress when undergoing morphogenetic processes, such as cell rearrangement. Here, we address the question in the Drosophila wing epithelium, where anisotropic tissue tension orients cell rearrangements. We found that anisotropic tissue tension localizes actin interacting protein 1 (AIP1), a cofactor of cofilin, on the remodeling junction via cooperative binding of cofilin to F-actin. AIP1 and cofilin promote actin turnover and locally regulate the Canoe-mediated linkage between actomyosin and the junction. This mechanism is essential for cells to resist the mechanical load imposed on the remodeling junction perpendicular to the direction of tissue stretching. Thus, the present study delineates how AIP1 and cofilin achieve an optimal balance between resistance to tissue tension and morphogenesis.
Highlights
In order to understand how tissue mechanics shapes animal body, it is critical to clarify how cells respond to and resist tissue stress when undergoing morphogenetic processes, such as cell rearrangement
Since the polygonal distribution of cells is much easier to measure than the dynamics of cell rearrangement, we used the fraction of hexagonal cells at 32 h after puparium formation (h APF), when the hexagonal cell packing process involving directional cell rearrangement is nearly complete, as a proxy for cell rearrangement defects
As described below, screening identified actin interacting protein 1 (AIP1), which promotes F-actin severing via cofilin[29,30,31,32], as a potential key regulator of cell rearrangement in the wing
Summary
In order to understand how tissue mechanics shapes animal body, it is critical to clarify how cells respond to and resist tissue stress when undergoing morphogenetic processes, such as cell rearrangement. Wing cells relocalize myosin-II (myo-II) at the adherens junction (AJ) that runs along the PD axis (PD junction) to resist tissue tension, and the balance between extrinsic stretching force and intrinsic cell junction tension favors PD cell rearrangement, thereby accelerating relaxation into a hexagonal cell pattern (hereafter called hexagonal cell packing; Supplementary Figure 1c, d)[7] This relaxation may be primarily driven through interface mechanics, consistent with the observation of shear-induced reconnection of interfaces and hexagonal lattice formation in foam, non-biological soft matter[27,28]. Our data illustrate that actin turnover ensures a resistance to anisotropic tissue tension and promotes directional cell rearrangement by reinforcing the structural stability of remodeling junctions. This proposed mechanism is likely to be relevant to development of other epithelial tissues in which tissue tension coordinates with morphogenetic signaling pathways in individual cells
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