Rag GTPases regulate TORC1 in nutrient response. This study identifies Rag GTPases as novel activators of TORC1 in response to amino acid signals. In Drosophila S2 cells, knockdown of Rag gene expression suppressed the stimulatory effect of amino acids on TORC1. Expression of constitutively active Rag in mammalian cells enhances TORC1 in the absence of amino acids, while dominant negative Rag blocks the stimulatory effects of amino acids on TORC1. Genetic studies in Drosophila show that Rag GTPases regulate cell growth, autophagy, and animal viability under starvation. These findings establish a novel function of Rag GTPases in TORC1 activation in response to amino acid signals. TORC1 is a critical regulator of cell growth and size, activated by various signals including amino acids. The study reveals that Rag GTPases are essential for TORC1 activation in response to amino acids. In Drosophila S2 cells, knockdown of dRagA and dRagC decreased dS6K phosphorylation. Constitutively active RagA and RagB increased S6K phosphorylation, while dominant negative RagA and RagB decreased it. These results indicate that Rag GTPases regulate TORC1 activity in response to amino acids. In mammalian cells, constitutively active RagA and RagB increased S6K phosphorylation, while dominant negative RagA and RagB decreased it. These findings suggest that Rag GTPases regulate TORC1 activity in response to amino acids. The study also shows that Rag GTPases regulate cell size in Drosophila. Expression of constitutively active dRagA increased cell size, while dominant negative dRagA decreased it. These results indicate that Rag GTPases regulate cell size in response to amino acids. The study also shows that Rag GTPases regulate autophagy in Drosophila. Overexpression of dRagA Q61L inhibited starvation-induced autophagy. These results indicate that Rag GTPases regulate autophagy in response to amino acids. The study further shows that Rag GTPases regulate nutrient response in Drosophila. Expression of dRagA Q61L increased cell size, while expression of dRagA T16N decreased it. These results indicate that Rag GTPases regulate nutrient response in Drosophila. The study also shows that Rag GTPases function independently and in parallel to promote TORC1 signaling. In mammalian cells, Rag functions upstream of mTOR. In Drosophila, Rag functions parallel or upstream of Rheb to stimulate cell growth. These results indicate that Rag GTPases regulate TORC1 signaling in response to amino acids. The study also shows that Rag GTPases regulate starvation responses in Drosophila. Overexpression of dRagA Q61Rag GTPases regulate TORC1 in nutrient response. This study identifies Rag GTPases as novel activators of TORC1 in response to amino acid signals. In Drosophila S2 cells, knockdown of Rag gene expression suppressed the stimulatory effect of amino acids on TORC1. Expression of constitutively active Rag in mammalian cells enhances TORC1 in the absence of amino acids, while dominant negative Rag blocks the stimulatory effects of amino acids on TORC1. Genetic studies in Drosophila show that Rag GTPases regulate cell growth, autophagy, and animal viability under starvation. These findings establish a novel function of Rag GTPases in TORC1 activation in response to amino acid signals. TORC1 is a critical regulator of cell growth and size, activated by various signals including amino acids. The study reveals that Rag GTPases are essential for TORC1 activation in response to amino acids. In Drosophila S2 cells, knockdown of dRagA and dRagC decreased dS6K phosphorylation. Constitutively active RagA and RagB increased S6K phosphorylation, while dominant negative RagA and RagB decreased it. These results indicate that Rag GTPases regulate TORC1 activity in response to amino acids. In mammalian cells, constitutively active RagA and RagB increased S6K phosphorylation, while dominant negative RagA and RagB decreased it. These findings suggest that Rag GTPases regulate TORC1 activity in response to amino acids. The study also shows that Rag GTPases regulate cell size in Drosophila. Expression of constitutively active dRagA increased cell size, while dominant negative dRagA decreased it. These results indicate that Rag GTPases regulate cell size in response to amino acids. The study also shows that Rag GTPases regulate autophagy in Drosophila. Overexpression of dRagA Q61L inhibited starvation-induced autophagy. These results indicate that Rag GTPases regulate autophagy in response to amino acids. The study further shows that Rag GTPases regulate nutrient response in Drosophila. Expression of dRagA Q61L increased cell size, while expression of dRagA T16N decreased it. These results indicate that Rag GTPases regulate nutrient response in Drosophila. The study also shows that Rag GTPases function independently and in parallel to promote TORC1 signaling. In mammalian cells, Rag functions upstream of mTOR. In Drosophila, Rag functions parallel or upstream of Rheb to stimulate cell growth. These results indicate that Rag GTPases regulate TORC1 signaling in response to amino acids. The study also shows that Rag GTPases regulate starvation responses in Drosophila. Overexpression of dRagA Q61