Abstract
The highly conserved complexes of Target of Rapamycin (TORC1 and TORC2) are central regulators to many vital cellular processes including growth and autophagy in response to nutrient availability. Previous research has extensively elucidated exogenous nutrient control on TORC1/TORC2; however, little is known about the potential alteration of nutrient pools from mutations in biosynthesis pathways and their impact on Tor pathway activity. Here, we analyze the impacts of heterozygous mutations in aromatic amino acid biosynthesis genes on TOR signaling via differential expression of genes downstream of TORC1 and autophagy induction for TORC1 and TORC2 activity.