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Vol. 16, No. 17, pp. 2286-2299, September 1, 2002

RESEARCH PAPER
Interactions between Ras1, dMyc, and dPI3K signaling in the developing Drosophila wing

David A. Prober,1 and Bruce A. Edgar2,3

1 Molecular and Cellular Biology Program, University of Washington, Seattle, Washington 98195, USA; 2 Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA

The Ras GTPase links extracellular signals to intracellular mechanisms that control cell growth, the cell cycle, and cell identity. An activated form of Drosophila Ras (RasV12) promotes these processes in the developing wing, but the effector pathways involved are unclear. Here, we present evidence indicating that RasV12 promotes cell growth and G1/S progression by increasing dMyc protein levels and activating dPI3K signaling, and that it does so via separate effector pathways. We also show that endogenous Ras is required to maintain normal levels of dMyc, but not dPI3K signaling during wing development. Finally, we show that induction of dMyc and regulation of cell identity are separable effects of Raf/MAPK signaling. These results suggest that Ras may only affect PI3K signaling when mutationally activated, such as in RasV12-transformed cells, and provide a basis for understanding the synergy between Ras and other growth-promoting oncogenes in cancer.

[Key Words: Ras; Myc; PI3K; Drosophila; cell growth; cell cycle]

3 Corresponding author.

GENES & DEVELOPMENT 16:2286-2299 © 2002 by Cold Spring Harbor Laboratory Press  ISSN 0890-9369/02 $5.00
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