Notch signalling is an evolutionarily conserved cell interaction mechanism, the role of which in controlling cell fate choices has been studied extensively. Recent studies in both vertebrates and invertebrates revealed additional functions of Notch in proliferation and apoptotic events. We provide evidence for an essential role of the Notch signalling pathway during morphogenetic cell movements required for the formation of the foregut-associated proventriculus organ in the Drosophila embryo. We demonstrate that the activation of the Notch receptor occurs in two rows of boundary cells in the proventriculus primordium. The boundary cells delimit a population of foregut epithelial cells that invaginate into the endodermal midgut layer during proventriculus morphogenesis. Notch receptor activation requires the expression of its ligand Delta in the invaginating cells and apical Notch receptor localisation in the boundary cells. We further show that the movement of the proventricular cells is dependent on the short stop gene that encodes the Drosophila plectin homolog of vertebrates and is a cytoskeletal linker protein of the spectraplakin superfamily. short stop is transcriptionally activated in response to the Notch signalling pathway in boundary cells and we demonstrate that the localisation of the Notch receptor and Notch signalling activity depend on short stop activity. Our results provide a novel link between the Notch signalling pathway and cytoskeletal reorganisation controlling cell movement during the development of foregut-associated organs.