![]() ![]() These results revealed that 2 molecular mechanisms, Npr2-Npr3-dependent GTP hydrolysis of Gtr1 and direct binding of Gtr2 to Kog1, are involved in TORC1 inactivation and autophagic induction.Ĭell growth is dynamically regulated in response to external cues such as nutrient availability, growth factor signals, and stresses. A GDP-bound Gtr1 mutant induced autophagy even under nutrient-rich conditions, and this effect was dependent on the direct binding of Gtr2 to Kog1. Furthermore, Gtr2 binds to the TORC1 subunit Kog1. Both npr2∆ mutants and a GTP-bound Gtr1 mutant suppressed autophagy and increased Tor1 vacuole localization. Npr2-Npr3 function upstream of Gtr1-Gtr2, homologs of the mammalian RRAG GTPase complex, which is crucial for TORC1 regulation. Their mammalian homologs, NPRL2 and NPR元, were also involved in regulation of autophagy. ![]() To investigate the mechanisms that regulate autophagy, we performed a genome-wide screen using a yeast deletion-mutant collection, and found that Npr2 and Npr3 mutants were defective in autophagy. Autophagy is an intracellular degradation process that delivers cytosolic material to lysosomes and vacuoles.
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