When the levels of intracellular amino acids are high, RRAG GTPases recruit 
MTORC1 to lysosomes and promote its activation. We found that RRAGs also recruit 
specific MTORC1 substrates to the lysosomal surface, thus facilitating 
MTORC1-mediated phosphorylation and regulation. In particular, active RRAGs 
interact with the transcription factor EB (TFEB), the master regulator of a gene 
network that promotes lysosomal biogenesis and autophagy. Redistribution to 
lysosomes is critical for MTORC1-dependent inactivation of TFEB under 
nutrient-rich conditions. Therefore, RRAGs play a critical role coordinating 
nutrient availability and cellular clearance.