Autophagy is an evolutionarily conserved pathway for the degradation of intracellular contents. How autophagy is regulated, especially upon changes in metabolic and nutritional state, remains poorly understood. By using a prototrophic strain of Saccharomyces cerevisiae, we observed that, unexpectedly, autophagy is strongly induced simply upon switch from a rich medium to a minimal medium in the complete absence of nitrogen starvation. This novel form of autophagy was termed "non-nitrogen-starvation (NNS)-induced autophagy." A visual screen uncovered three regulators of autophagy-Iml1p, Npr2p, and Npr3p-which function in the same complex and are selectively required for NNS-induced autophagy. During NNS-induced autophagy, Iml1p localized to either preautophagosomal structures (PAS) or non-PAS punctate structures. This localization suggests that Iml1p or the Iml1p-Npr2p-Npr3p complex might regulate autophagosome formation. Ultrastructural analysis confirmed that autophagosome formation was strongly impaired in ?iml1, ?npr2, and ?npr3 cells during NNS-induced autophagy. Moreover, Iml1p contains a conserved domain that is required for NNS-induced autophagy as well as complex formation. Collectively, our findings have revealed the existence of additional mechanisms that regulate autophagy under previously unrecognized conditions, in response to relatively more subtle changes in metabolic and nutritional state.
|Evidence ID||Analyze ID||Interactor||Interactor Systematic Name||Interactor||Interactor Systematic Name||Type||Assay||Annotation||Action||Modification||Phenotype||Source||Reference||Note|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Gene Ontology Term||Gene Ontology Term ID||Qualifier||Aspect||Method||Evidence||Source||Assigned On||Reference||Annotation Extension|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Phenotype||Experiment Type||Experiment Type Category||Mutant Information||Strain Background||Chemical||Details||Reference|
|Evidence ID||Analyze ID||Regulator||Regulator Systematic Name||Target||Target Systematic Name||Experiment||Conditions||Strain||Source||Reference|