Forces generated by the actomyosin cytoskeleton are key contributors to many morphogenetic processes. The actomyosin cytoskeleton organises in different types of networks depending on intracellular signals and on cell-cell and cell-extracellular matrix (ECM) interactions. However, actomyosin networks are not static and transitions between them have been proposed to drive morphogenesis. Still, little is known about the mechanisms that regulate the dynamics of actomyosin networks during morphogenesis. This work uses the Drosophila follicular epithelium, real-time imaging, laser ablation and quantitative analysis to study the role of integrins on the regulation of basal actomyosin networks organisation and dynamics and the potential contribution of this role to cell shape. We find that elimination of integrins from follicle cells impairs F-actin recruitment to basal medial actomyosin stress fibers. The available F-actin redistributes to the so-called whip-like structures, present at tricellular junctions, and into a new type of actin-rich protrusions that emanate from the basal cortex and project towards the medial region. These F-actin protrusions are dynamic and changes in total protrusion area correlate with periodic cycles of basal myosin accumulation and constriction pulses of the cell membrane. Finally, we find that follicle cells lacking integrin function show increased membrane tension and reduced basal surface. Furthermore, the actin-rich protrusions are responsible for these phenotypes as their elimination in integrin mutant follicle cells rescues both tension and basal surface defects. We thus propose that the role of integrins as regulators of stress fibers plays a key role on controlling epithelial cell shape, as integrin disruption promotes reorganisation into other types of actomyosin networks, in a manner that interferes with proper expansion of epithelial basal surfaces.

由放线菌素细胞骨架产生的力是许多形态发生过程的关键因素。根据细胞内信号以及细胞-细胞和细胞-细胞外基质（ECM）的相互作用，放线菌素的细胞骨架组织在不同类型的网络中。然而，放线菌素网络不是静态的，并且已经提出它们之间的过渡来驱动形态发生。仍然很少有人了解在形态发生过程中调节肌动球蛋白网络动态的机制。这项工作使用果蝇滤泡上皮细胞，实时成像，激光消融和定量分析，以研究整联蛋白在调节基础肌动球蛋白网络组织和动力学中的作用以及这种作用对细胞形态的潜在贡献。我们发现，从卵泡细胞中消除整合素会损害F-肌动蛋白募集至基底内侧肌动球蛋白应激纤维。可用的F-肌动蛋白重新分布在三细胞交界处的所谓的鞭状结构中，并重新分布成一种新的富含肌动蛋白的突起，这种突起从基底皮层发出并向内侧区域突出。这些F-肌动蛋白突起是动态的，总突起面积的变化与基础肌球蛋白积累和细胞膜收缩脉冲的周期性循环相关。最后，我们发现缺乏整联蛋白功能的卵泡细胞显示增加的膜张力和减少的基底表面。此外，富含肌动蛋白的突起负责这些表型，因为它们在整合素突变型卵泡细胞中的消除可消除张力和基底表面缺陷。因此，我们提出整联蛋白作为应激纤维调节剂的作用在控制上皮细胞形状方面起着关键作用，因为整联蛋白的破坏促进了重组为其他类型的肌动球蛋白网络，从而干扰了上皮基底表面的适当扩展。