The phenomenon of tissue fluidity—cells’ ability to rearrange relative to each other in confluent tissues—has been linked to several morphogenetic processes and diseases, yet few molecular regulators of tissue fluidity are known. Ommatidial rotation (OR), directed by planar cell polarity signaling, occurs during Drosophila eye morphogenesis and shares many features with polarized cellular migration in vertebrates. We utilize in vivo live imaging analysis tools to quantify dynamic cellular morphologies during OR, revealing that OR is driven autonomously by ommatidial cell clusters rotating in successive pulses within a permissive substrate. Through analysis of a rotation-specific nemo mutant, we demonstrate that precise regulation of junctional E-cadherin levels is critical for modulating the mechanical properties of the tissue to allow rotation to progress. Our study defines Nemo as a molecular tool to induce a transition from solid-like tissues to more viscoelastic tissues broadening our molecular understanding of tissue fluidity.

组织流动性现象——细胞在汇合组织中相对于彼此重新排列的能力——与几种形态发生过程和疾病有关，但组织流动性的分子调节剂知之甚少。Ommatidial 旋转 (OR)，由平面细胞极性信号指示，发生在果蝇眼形态发生过程中，与脊椎动物的极化细胞迁移有许多共同特征。我们利用体内实时成像分析工具来量化 OR 期间的动态细胞形态，揭示 OR 是由在允许基质内以连续脉冲旋转的小眼细胞簇自主驱动的。通过分析特定于轮换的nemo突变体，我们证明精确调节连接 E-钙粘蛋白水平对于调节组织的机械特性以允许旋转进行是至关重要的。我们的研究将 Nemo 定义为一种分子工具，可诱导从固体样组织转变为更具粘弹性的组织，拓宽了我们对组织流动性的分子理解。