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In multicellular organisms, growth and proliferation is adjusted to nutritional conditions by a complex signaling network. The Insulin receptor/target of rapamycin (InR/TOR) signaling cascade plays a pivotal role in nutrient dependent growth regulation in  Drosophila  and mammals alike. Here we identify Cyclin G (CycG) as a regulator of growth and metabolism in  Drosophila .  CycG  mutants have a reduced body size and weight and show signs of starvation accompanied by a disturbed fat metabolism. InR/TOR signaling activity is impaired in  cycG  mutants, combined with a reduced phosphorylation status of the kinase Akt1 and the downstream factors S6-kinase and eukaryotic translation initiation factor 4E binding protein (4E-BP). Moreover, the expression and accumulation of  Drosophila  insulin like peptides (dILPs) is disturbed in  cycG  mutant brains. Using a reporter assay, we show that the activity of one of the first effectors of InR signaling, Phosphoinositide 3-kinase (PI3K92E), is unaffected in  cycG  mutants. However, the metabolic defects and weight loss in  cycG  mutants were rescued by overexpression of Akt1 specifically in the fat body and by mutants in  widerborst  ( wdb ), the B'-subunit of the phosphatase PP2A, known to downregulate Akt1 by dephosphorylation. Together, our data suggest that CycG acts at the level of Akt1 to regulate growth and metabolism via PP2A in  Drosophila .

Cyclin G Functions as a Positive Regulator of Growth and Metabolism in Drosophila