The Ras GTPase links extracellular mitogens to intracellular mechanisms tha
t control cell proliferation. To understand how Ras regulates proliferation
in vivo, we activated or inactivated Ras in cell clones in the developing
Drosophila wing. Cells lacking Ras were smaller, had reduced growth rates,
accumulated in G1, and underwent apoptosis due to cell competition. Convers
ely, activation of Ras increased cell size and growth rates and promoted G1
/S transitions. Ras upregulated the growth driver dMyc, and both Pas and dM
yc increased levels of cyclin E posttranscriptionally. We propose that Pas
primarily promotes growth and that growth is coupled to G1/S progression vi
a cyclin E. Interestingly, upregulation of growth by Pas did not deregulate
G2/M progression or a developmentally regulated cell cycle exit.