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The TOR protein kinases (TOR1 and TOR2 in yeast; mTOR/FRAP/RAFT1 in mammals) promote cellular proliferation in response to nutrients and growth factors, but their role in development is poorly understood. Here, we show that the  Drosophila  TOR homolog  dTOR  is required cell autonomously for normal growth and proliferation during larval development, and for increases in cellular growth caused by activation of the phosphoinositide 3-kinase (PI3K) signaling pathway. As in mammalian cells, the kinase activity of dTOR is required for growth factor-dependent phosphorylation of p70 S6 kinase (p70 S6K ) in vitro, and we demonstrate that overexpression of p70 S6K  in vivo can rescue  dTOR  mutant animals to viability. Loss of  dTOR  also results in cellular phenotypes characteristic of amino acid deprivation, including reduced nucleolar size, lipid vesicle aggregation in the larval fat body, and a cell type-specific pattern of cell cycle arrest that can be bypassed by overexpression of the S-phase regulator cyclin E. Our results suggest that  dTOR  regulates growth during animal development by coupling growth factor signaling to nutrient availability.

Regulation of cellular growth by the Drosophila target of rapamycin dTOR