The red-eared slider turtle, can survive 3-4 months of anoxic submergence in cold water during the winter. The effect of hypoxia/anoxia on protein synthesis in the turtle was investigated with a focus on the insulin-signaling pathway and analysis of the mammalian target of rapamycin (mTOR) and its upstream and downstream effectors in liver and white muscle. Expression of mTORC1 did not change in muscle but increased significantly in liver after 5 and 20 hours of anoxic submergence. Upstream effectors, AKT and RAPTOR, were also elevated in liver but suppressed in muscle. PRAS40 and TSC2
inhibitors of mTOR were differentially regulated in both tissues but generally suppressed. Downstream targets of mTOR signaling (eIF4E, 4E-BP1, P70S6K, S6) as well as the poly(A) binding protein also showed differential responses to anoxia. Overall, the data indicate that the early response to anoxia is maintenance of protein synthesis in liver but suppression in white muscle.