Abstract
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 MTs networks is still unclear. Here, we show that MT-dependent intracellular trafficking has 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 intracellular trafficking impairs apicomedial myosin formation and apical constriction. We show that MTs and dynein motors regulate Fog signaling activity. We further show that MTs are required for apical enrichment of key apical and junctional proteins in the SG, including the apical determinant protein Crumbs (Crb), the key adherens junction protein E-Cadherin (E-Cad) and the scaffolding protein Bazooka/Par3. Targeted knockdown of these genes in the SG disrupts apical myosin networks and results in apical constriction defects. Our data suggests a role of MT-dependent intracellular trafficking in regulating actomyosin networks and cell junctions, to coordinate cell behaviors during tubular organ formation.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
The title of the manuscript and the text have been slightly modified.