Protein synthesis upon acute nutrient restriction relies on proteasome function.
The mechanisms that protect mammalian cells against amino acid deprivation are only partially understood. We found that during an acute decrease in external amino acid supply, before up-regulation of the autophagosomal-lysosomal pathway, efficient translation was ensured by proteasomal protein degradation. Amino acids for the synthesis of new proteins were supplied by the degradation of preexisting proteins, whereas nascent and newly formed polypeptides remained largely protected from proteolysis. Proteasome inhibition during nutrient deprivation caused rapid amino acid depletion and marked impairment of translation. Thus, the proteasome plays a crucial role in cell survival after acute disruption of amino acid supply.
Vabulas
Ramunas M
RM
Department of Cellular Biochemistry, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D-82152 Martinsried, Germany. vabulas@biochem.mpg.de
Hartl
F Ulrich
FU
D000596:Amino Acids / Q000378:metabolism*; D001383:Azetidinecarboxylic Acid / Q000378:metabolism; D002460:Cell Line; D049452:Green Fluorescent Proteins / Q000235:genetics; D006367:HeLa Cells; D006801:Humans; D046988:Proteasome Endopeptidase Complex / Q000502:physiology*; D061988:Proteasome Inhibitors; D014176:Protein Biosynthesis / Q000502:physiology*; D011494:Protein Kinases / Q000378:metabolism; D025801:Ubiquitin / Q000235:genetics
D000596:Amino Acids; D061988:Proteasome Inhibitors; D025801:Ubiquitin; D049452:Green Fluorescent Proteins; D001383:Azetidinecarboxylic Acid; D011494:Protein Kinases; D046988:Proteasome Endopeptidase Complex