| 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 evolutionary conserved Target of Rapamycin signalling (TOR) in mediating collective cell movement employing the model of migrating BCs in Drosophila oogenesis. Though TOR signalling is classically linked to cell growth, cell proliferation and metabolism, here we demonstrate TOR Complex1 (TORC1) regulates efficient group cell movement of BCs. Employing live cell imaging, genetics, and tissue immunohistochemistry, we demonstrate TOR functions through transcription factor Reptor to modulate the 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 DIAP-1 homolog, Baculoviral IAP repeat-containing 2 (BIRC2), similar to what is observed in flies.
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