Target of Rapamycin Complex 1 (TORC1) is a master regulator of metabolism in eukaryotes that integrates information from multiple upstream signaling pathways. The evolutionary conserved complex Gap activity towards Rags (GATOR) inhibits TORC1 activity in response to amino acid limitation. In yeast, GATOR1 mutants show proliferation defects during nitrogen source scarcity, but not when cultured in nutrient rich conditions. In humans, the GATOR1 complex has been implicated in a wide array of human pathologies including cancer and hereditary forms of epilepsy. These observations strongly suggest that in metazoans the GATOR1 complex has acquired functions beyond coordinating a response to amino acid limitation. However, the precise requirement of GATOR1 in animal physiology remains largely undefined. Here we generate null mutants of the GATOR1 components nprl2, nprl3 and iml1 in Drosophila. We find that all three mutants have inappropriately high TORC1 activity. Moreover the GATOR1 mutants are semi-lethal with a percentage of homozygous animals dying as pharate adults. Notably, the nprl2 and nprl3 mutant adults exhibit profound ataxia. This ataxia is metabolic in origin in that it is rescued by the expression of Nprl3 in the fat body, but not muscles or neurons, of nprl3 mutants. Consistent with the theory that inhibiting TORC1 activity extends lifespan, the nprl2 and nprl3 mutants have shortened lifespan. Finally, our data confirm that in addition to its role in the development and physiology of Drosophila raised under standard culture conditions, the GATOR1 complex has retained a critical role in the response to nutrient stress. Notably, nprl2 and nprl3 mutants fail to activate autophagy in response to amino acid stress and are extremely sensitive to both amino acid and complete starvation. In summary we find that the TORC1 inhibitor GATOR1 contributes to multiple aspects of the development and physiology of Drosophila.