TOR signalling regulates epithelial cell shape transition in Drosophila oogenesis

Epithelial morphogenesis plays an important role in form generation, organ development, and maintenance of adult tissues in the metazoans. Given its wide implication, aberrant morphogenesis is linked to severe developmental defects and in a few instances also associated with tumorigenesis. Employing the model of Drosophila oogenesis, we have examined the role of the evolutionary conserved Target of Rapamycin (TOR) kinase pathway, a known regulator of cell growth and size in mediating shape transition of cuboidal cells to squamous epithelial fate. Utilizing genetic tools, immunohistochemistry, and live cell imaging, we demonstrate that TOR signaling is active and required for epithelial morphogenesis during Drosophila oogenesis. Further, loss of function analyses indicates that non-canonical TOR signaling functions through PAR-1 to mediate the removal of lateral cell adhesion molecule, Fasciclin 2, to allow proper squamous cell morphogenesis. In addition, we demonstrate the effect of TOR through PAR-1 on cell shape transition is mediated via the modulation of endocytosis. Overall, our data give novel insight into how TOR signaling mediates cell shape transition during epithelial morphogenesis in the metazoans.