Epithelial folding is typically driven by localized actomyosin contractility. However, it remains unclear how epithelia deform when myosin levels are low and uniform. In the Drosophila gastrula, dorsal fold formation occurs despite a lack of localized myosin changes, while the fold-initiating cells reduce cell height following basal shifts of polarity via an unknown mechanism. We show that cell shortening depends on an apical microtubule network organized by the CAMSAP protein Patronin. Prior to gastrulation, microtubule forces generated by the minus-end motor dynein scaffold the apical cell cortex into a dome-like shape, while the severing enzyme Katanin facilitates network remodelling to ensure tissue-wide cell size homeostasis. During fold initiation, Patronin redistributes following basal polarity shifts in the initiating cells, apparently weakening the scaffolding forces to allow dome descent. The homeostatic network that ensures size/shape homogeneity is thus repurposed for cell shortening, linking epithelial polarity to folding via a microtubule-based mechanical mechanism.

中文翻译：

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稳态的根尖微管网络通过基础极性转移缩短了用于上皮折叠的细胞。

上皮折叠通常由局部肌动球蛋白收缩力驱动。然而，尚不清楚当肌球蛋白水平低且均匀时上皮细胞如何变形。在果蝇的腹果蝇中，尽管缺乏局部的肌球蛋白变化，但仍发生背褶形成，而起褶皱的细胞由于未知机制通过极性的基础转移而降低了细胞高度。我们显示细胞缩短取决于由CAMSAP蛋白Patronin组织的顶端微管网络。在胃造气之前，负端运动动力蛋白产生的微管力将心尖细胞皮层构筑成圆顶状，而切断酶Katanin促进网络重塑，以确保组织范围内细胞大小的体内​​平衡。在折叠起始过程中，Patronin在起始细胞的基础极性转移后重新分布，显然削弱了脚手架的力量，使穹顶下降。确保大小/形状均匀性的稳态网络因此被重新用于细胞缩短，通过基于微管的机械机制将上皮极性连接到折叠。