Autophagy is a bulk protein degradation process that is induced by starvation. The control mechanism for induction of autophagy is not well understood. We found that Tor, a @entity4357 kinase homologue, is involved in the control of autophagy in the @entity375 , @entity375 . When @entity3446 , an inhibitor of Tor function, is added, autophagy is induced even in cells growing in nutrient-rich medium. A temperature-sensitive tor mutant also leads to induction of autophagy at a nonpermissive temperature. These results indicate that Tor negatively regulates the induction of autophagy. Tor is the first molecule that is identified as a pivotal player in the starvation-signaling pathway of autophagy. Furthermore, we found that a high concentration of @entity268 is inhibitory for induction of autophagy. APG gene products are involved in autophagy induced by starvation. Autophagy was not induced in apg mutants in the presence of @entity3446 , indicating that the site of action of Tor is upstream of those of Apg proteins. In nutrient-rich medium, Apg proteins are involved also in the transport of aminopeptidase I from the cytosol to the vacuole. Tor may act to switch Apg function between autophagy and transport of aminopeptidase I.

Tor, a XXXX kinase homologue, controls autophagy in @entity375 .

@entity3446 :: ('MESH:D020123', 'Chemical') :: ['rapamycin'] @entity375 :: ('4932', 'Species') :: ['yeast', 'Saccharomyces cerevisiae'] @entity268 :: ('CHEBI:17489', 'Chemical') :: ['cAMP'] @entity4357 :: ('MESH:D010716', 'Chemical') :: ['phosphatidylinositol']
@entity4357 :: (MESH:D010716,Chemical) :: ['phosphatidylinositol']
