Precise regulation of cell shape is vital for building functional tissues. Here, we study the mechanisms that lead to the formation of highly elongated anisotropic epithelial cells in the Drosophila epidermis. We demonstrate that this cell shape is the result of two counteracting mechanisms at the cell surface that regulate the degree of elongation: actomyosin, which inhibits cell elongation downstream of RhoA (Rho1 in Drosophila) and intercellular adhesion, modulated via clathrin-mediated endocytosis of E-cadherin (encoded by shotgun in flies), which promotes cell elongation downstream of the GTPase Arf1 (Arf79F in Drosophila). We show that these two mechanisms do not act independently but are interconnected, with RhoA signalling reducing Arf1 recruitment to the plasma membrane. Additionally, cell adhesion itself regulates both mechanisms – p120-catenin, a regulator of intercellular adhesion, promotes the activity of both Arf1 and RhoA. Altogether, we uncover a complex network of interactions between cell–cell adhesion, the endocytic machinery and the actomyosin cortex, and demonstrate how this network regulates cell shape in an epithelial tissue in vivo.

细胞形状的精确调节对于构建功能组织至关重要。在这里，我们研究导致果蝇表皮中高度伸长的各向异性上皮细胞形成的机制。我们证明，这种细胞形状是细胞表面调节伸长程度的两种抵消机制的结果：肌动球蛋白，它抑制 RhoA（果蝇中的 Rho1）下游的细胞伸长和细胞间粘附，通过网格蛋白介导的 E 的内吞作用进行调节-钙粘蛋白（果蝇中由鸟枪编码），促进 GTPase Arf1（果蝇中的 Arf79F ）下游的细胞伸长。我们发现这两种机制并不是独立作用而是相互关联的，RhoA 信号传导减少了 Arf1 向质膜的募集。此外，细胞粘附本身调节这两种机制 - p120-连环蛋白（细胞间粘附的调节剂）可促进 Arf1 和 RhoA 的活性。总而言之，我们揭示了细胞间粘附、内吞机制和肌动球蛋白皮层之间相互作用的复杂网络，并证明了该网络如何调节体内上皮组织中的细胞形状。