A homeostatic apical microtubule network shortens cells for epithelial folding via a basal polarity shift
A homeostatic apical microtubule network shortens cells for epithelial folding via a basal polarity shift
复制标题
DOI：
10.1038/s41556-017-0001-3
复制
发表时间：
2017-12
影响因子：
21.3
通讯作者：
Michiko Takeda;M. M. Sami-M.;Yu-Chiun Wang
中科院分区：
文献类型：
--
作者：
Michiko Takeda;M. M. Sami-M.;Yu-Chiun Wang
上皮折叠通常是由局部肌动球蛋白收缩性驱动的。然而，当肌球蛋白水平低且均匀时，上皮如何变形尚不清楚。在果蝇中，尽管缺乏局部肌球蛋白变化，但仍会发生背褶皱的形成，而褶皱启动细胞通过未知的机制在极性基础转移后降低细胞高度。我们发现细胞缩短依赖于由CAMSAP蛋白Patronin组织的顶端微管网络。在原肠形成之前，由负端运动动力蛋白产生的微管力将顶端细胞皮层支架成圆顶状，而切断酶Katanin促进网络重塑以确保组织范围内细胞大小的稳态。在折叠起始过程中，随着起始细胞的基本极性变化，光顾蛋白重新分布，显然削弱了支架力以允许圆顶下降。因此，确保大小/形状均匀性的稳态网络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与折叠联系起来。
Epithelial folding is typically driven by localized actomyosin contractility. However, it remains unclear how epithelia deform when myosin levels are low and uniform. In theDrosophilagastrula, 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.