The expulsion of dying epithelial cells requires well-orchestrated remodelling steps to maintain tissue sealing. This process, named cell extrusion, has been mostly analysed through the study of actomyosin regulation. Yet, the mechanistic relationship between caspase activation and cell extrusion is still poorly understood. Using the Drosophila pupal notum, a single layer epithelium where extrusions are caspase-dependent, we showed that the initiation of cell extrusion and apical constriction are surprisingly not associated with the modulation of actomyosin concentration and dynamics. Instead, cell apical constriction is initiated by the disassembly of a medio-apical mesh of microtubules which is driven by effector caspases. Importantly, the depletion of microtubules is sufficient to bypass the requirement of caspases for cell extrusion, while microtubule stabilisation strongly impairs cell extrusion. This study shows that microtubules disassembly by caspases is a key rate-limiting step of extrusion, and outlines a more general function of microtubules in epithelial cell shape stabilisation.

排出垂死的上皮细胞需要精心策划的重塑步骤以维持组织密封。这个过程，称为细胞挤压，主要通过肌动球蛋白调节的研究来分析。然而，半胱天冬酶激活和细胞挤出之间的机制关系仍然知之甚少。使用果蝇pupal notum 是一种单层上皮，其中挤出依赖于半胱天冬酶，我们发现细胞挤出和顶端收缩的开始与肌动球蛋白浓度和动力学的调节无关。相反，细胞顶端收缩是由由效应半胱天冬酶驱动的中间顶端微管网的分解引发的。重要的是，微管的消耗足以绕过半胱天冬酶对细胞挤压的要求，而微管稳定会严重损害细胞挤压。该研究表明，半胱天冬酶对微管的分解是挤出的关键限速步骤，并概述了微管在上皮细胞形状稳定中的更一般功能。