Our results suggest that Ceng1A plays a previously not described role in regulating developmental timing independent of nutrient conditions, resulting in reduced ecdysone signaling. IlS and AMPK exert an important function under unfavorable conditions. Increased sensitivity towards IlS leads to a limited capability to cope with nutrient restricted conditions. Tetrodotoxin citrate mutants with increased sensitivity towards IlS or AMPK mutants are not able to adapt to nutrition-limited conditions and therefore do not reduce their metabolic rate, leading to a rapid exhaustion of fat stores. This results in decreased survival of those mutants compared to their wildtype counterparts raised under the same conditions. To test if ceng1A mutants are sensitive to such stress conditions, we maintained five-day old adult flies on nutrient depleted media. The survival time of ceng1A mutants, however, was not changed significantly. In summary, our results indicate that Ceng1A does not have a major impact on IlS or AMPK signaling. Since growth, survival or IlS-dependent target gene expression were not affected in ceng1A mutants, we tested whether Ceng1A is required for metabolic control, in a manner similar to PIKE-A, which involves regulation of fat storage and mobilization: PIKE whole body knockout mice are leaner and display a significant reduction in white adipose tissue and an increase in b-oxidation. We investigated body fat content in ceng1A mutant flies using thin layer chromatography. We measured whole body triacylglyceride levels at three different time points during the starvation experiment. Neither at the beginning nor during the starvation period ceng1A mutants showed obvious body fat mass differences compared to control flies. Consequently, we did not observe an induction of lipase3 expression, another starvation marker, under normal feeding conditions, indicating that lipid mobilization is not altered in the mutants. PIKE 2/2 mice are resistant to high-fat diet-induced obesity due to inhibited adipocyte differentiation. We analyzed fat tissue Daminozide morphology of ceng1A and w2 larvae under normal and high-fat conditions. To this end, larvae were grown on standard or high-fat diet and third instar fat bodies were isolated and stained with Oil Red O. Under both conditions no difference in fat body morphology or lipid droplet storage could be observed in ceng1A mutants compared to larvae.