Tuberous sclerosis complex 1 (PvTSC1) participates in ammonia nitrogen induced oxidative stress in Penaeus vannamei by regulating autophagy

The tuberous sclerosis complex 1 (TSC1) is a critical upstream regulator of autophagy. Nevertheless, the detailed molecular mechanism of TSC1 and its function in crustacean are still not well understood. In the present study, TSC1 was identified and characterized from Penaeus vannamei. Molecular feature analysis revealed that the open reading frame (ORF) of PvTSC1 was 3516 bp encoding a polypeptide of 1172 amino acids with a conserved N-terminal hamartin domain and two coiled-coil region domains in the C-terminus. The homologous alignment showed that the amino acid sequence of PvTSC1 shared 28.17% ~ 59.25% identity with that of TSC1 in other species. The mRNA transcripts of PvTSC1 were found in all detected tissues of shrimp, and PvTSC1 was mainly located in the cytoplasm of hemocytes. Antioxidant enzyme and PvTSC1 were significantly up-regulated in hemocytes, gill and hepatopancreas after high ammonia nitrogen stress. After PvTSC1 silencing, ROS accumulation increased and autophagy production decreased significantly. And the expression level of PvmTOR was increased significantly, on the contrary, autophagy-related genes (PvATG14 and PvBeclin-1) were decreased significantly. Finally, the mortality of shrimp increased significantly in the PvTSC1-silenced shrimp. These results indicated that ammonia nitrogen had a significant effect on oxidative stress injury of shrimp, and autophagy was a remarkable survival mechanism of shrimp with oxidative stress injury regulated by PvTSC1.