The formation of an epithelial tube is a fundamental process for organogenesis. During Drosophila embryonic salivary gland (SG) invagination, Folded gastrulation (Fog)-dependent Rho-associated kinase (Rok) promotes contractile apical myosin formation to drive apical constriction. Microtubules (MTs) are also crucial for this process and are required for forming and maintaining apicomedial myosin. However, the underlying mechanism that coordinates actomyosin and MT networks still remains elusive. Here, we show that MT-dependent intracellular trafficking regulates apical constriction during SG invagination. Key components involved in protein trafficking, such as Rab11 and Nuclear fallout (Nuf), are apically enriched near the SG invagination pit in a MT-dependent manner. Disruption of the MT networks or knockdown of Rab11 impairs apicomedial myosin formation and apical constriction. We show that MTs and Rab11 are required for apical enrichment of the Fog ligand and the continuous distribution of the apical determinant protein Crumbs (Crb) and the key adherens junction protein E-Cadherin (E-Cad) along junctions. Targeted knockdown of crb or E-Cad in the SG disrupts apical myosin networks and results in apical constriction defects. Our data suggest a role of MT- and Rab11-dependent intracellular trafficking in regulating actomyosin networks and cell junctions, to coordinate cell behaviors during tubular organ formation.

中文翻译：

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在组织内陷过程中通过微管和Rab11依赖性的根尖运输调节根尖收缩

上皮管的形成是器官发生的基本过程。在果蝇胚胎唾液腺（SG）内陷过程中，依赖于折叠胃（Fog）的Rho相关激酶（Rok）促进收缩性心尖肌球蛋白的形成，从而驱动心尖收缩。微管（MTs）在此过程中也至关重要，并且是形成和维持蜂巢肌球蛋白所必需的。但是，协调肌动球蛋白和MT网络的基本机制仍然难以捉摸。在这里，我们显示MT依赖细胞内运输调节SG内陷过程中的根尖收缩。涉及蛋白质贩运的关键成分，如Rab11和核沉降（Nuf），以MT依赖性方式在SG侵入坑附近顶端富集。MT网络的破坏或Rab11的敲低削弱了apiededial肌球蛋白的形成和根尖收缩。我们显示MTs和Rab11是Fog配体的顶端富集和顶端决定簇蛋白Crmbs（Crb）和关键粘附连接蛋白E-Cadherin（E-Cad）沿连接的连续分布所必需的。在SG中有针对性地抑制crb或E-Cad会破坏顶端肌球蛋白网络，并导致顶端收缩缺陷。我们的数据表明依赖MT和Rab11的细胞内运输在调节肌动球蛋白网络和细胞连接，以协调肾小管器官形成过程中的细胞行为中的作用。我们显示MTs和Rab11是Fog配体的顶端富集和顶端决定簇蛋白Crmbs（Crb）和关键粘附连接蛋白E-Cadherin（E-Cad）沿连接的连续分布所必需的。在SG中有针对性地抑制crb或E-Cad会破坏顶端肌球蛋白网络，并导致顶端收缩缺陷。我们的数据表明依赖MT和Rab11的细胞内运输在调节肌动球蛋白网络和细胞连接，以协调肾小管器官形成过程中的细胞行为中的作用。我们显示MTs和Rab11是Fog配体的顶端富集和顶端决定簇蛋白Crmbs（Crb）和关键粘附连接蛋白E-Cadherin（E-Cad）沿连接的连续分布所必需的。在SG中有针对性地抑制crb或E-Cad会破坏顶端肌球蛋白网络，并导致顶端收缩缺陷。我们的数据表明依赖MT和Rab11的细胞内运输在调节肌动球蛋白网络和细胞连接，以协调肾小管器官形成过程中的细胞行为中的作用。