摘要：SummaryMYCT1 has been shown to function as a tumor suppressor in various tumors, but its role in metabolism has never been reported. Here, we showed that global inactivation of Myct1 in mice led to progressive accumulation of glycogen in the liver, which was accompanied by aberrant changes in intermediates of the glycogen metabolic pathway. Mechanistically, MYCT1 appeared to promote translation efficiency of PGM1, UGP2 and GSK3A in hepatic cells in a RACK1-dependent manner. Consequently, upregulation of the three enzymes enhanced the glycogen shunt. Our data reveal a critical role of MYCT1 as a switch for the glycogen shunt in tumor cells.Graphical abstractDisplay OmittedHighlights•Myct1depletion causes glycogen accumulation in mouse liver•MYCT1 affects glycogen shunt in tumor and normal cells•MYCT1 regulates translation efficiency of glycogen enzymes•MYCT1 alters the glycogen shunt in a RACK1 dependent mannerPhysiology; Animal physiology; Molecular biology
