Journal
CELL
Volume 100, Issue 4, Pages 435-446Publisher
CELL PRESS
DOI: 10.1016/S0092-8674(00)80679-0
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Funding
- NCI NIH HHS [5P30CA15704-26] Funding Source: Medline
- NIGMS NIH HHS [GM51186] Funding Source: Medline
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The Ras GTPase links extracellular mitogens to intracellular mechanisms that 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. Conversely, activation of Ras increased cell size and growth rates and promoted G1/S transitions. Ras upregulated the growth driver dMyc, and both Pas and dMyc increased levels of cyclin E posttranscriptionally. We propose that Pas primarily promotes growth and that growth is coupled to G1/S progression via cyclin E. Interestingly, upregulation of growth by Pas did not deregulate G2/M progression or a developmentally regulated cell cycle exit.
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