Microtubules regulate intracellular trafficking to mediate apical constriction during tissue invagination
The Drosophila embryonic salivary gland (SG) invaginates by budding to form a three-dimensional tube. Coordinated apical constriction during SG invagination is critical for proper tube shape. We previously showed that Folded gastrulation (Fog)-dependent Rho-associated kinase (Rok) accumulation in the apicomedial region of the SG cells is required for apicomedial myosin formation and clustered apical constriction near the invagination pit. Here, we show that microtubule (MT)-dependent intracellular trafficking has a role in regulating apical constriction during SG invagination. Key components involved in protein trafficking, including dynein heavy chain, Rab11 and Nuclear fallout (Nuf), are apically enriched near the invagination pit in a MT-dependent manner during SG invagination. This enrichment is crucial for apical constriction as disruption of the MT networks or intracellular trafficking impairs formation of apicomedial myosin, which leads to apical constriction defects. We show that apical transport of several proteins along MTs, either in a Rab11-dependent or independent manner, mediates clustered apical constriction during SG invagination. Key proteins that are transported include the Fog ligand, the apical determinant protein Crb, the key adherens junction protein E-Cad and the scaffolding protein Bazooka/Par3, and knockdown of these genes in the SG results in apical constriction defects. These results define a role of MT-dependent intracellular trafficking in regulating the actomyosin networks ands cell junctions to coordinate cell behaviors during tubular organ formation.