Abstract
Collective cell migration is seen in various biological processes spanning embryonic development, organogenesis, wound healing and, unfortunately, cancer metastasis. Here, we have examined the role of the evolutionarily conserved Target of Rapamycin signalling (TOR) in mediating collective cell movement employing the model of migrating border cells (BCs) in Drosophila oogenesis. Although TOR signalling is classically linked to cell growth, cell proliferation and metabolism, here we demonstrate that TOR complex 1 (TORC1) regulates efficient group cell movement of BCs. Employing live cell imaging, genetics, and tissue immunohistochemistry, we demonstrate that TOR functions through the transcription factor REPTOR to modulate Death-associated inhibitor of apoptosis 1 (Diap1) in mediating efficient movement of BCs. Coincidentally, rapamycin-treated myeloblast Kasumi-1 cells exhibit lower levels of transcript for the Diap1 homologue baculoviral IAP repeat-containing 2 (BIRC2), similar to what is observed in flies.