Tor-mediated induction of autophagy via an Apg1 protein kinase complex
What this study shows
The founding experiment of the whole TOR-to-autophagy axis. Starvation or rapamycin raises the kinase activity of Apg1 (the yeast counterpart of ULK1), and TOR keeps autophagy off by holding Apg13 hyperphosphorylated so that it cannot bind and activate Apg1. Boundary: yeast only, and the mammalian version of the same step (ULK1-ATG13-FIP200) was shown separately nine years later.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Saccharomyces cerevisiae (yeast)) rather than a whole-organism health-outcome study. That is often exactly where causal biology gets established -- the code says which system the finding was shown in, and nothing about how good the work is. |
| Study type | 5 - Mechanistic / In Vitro |
| Model system | Saccharomyces cerevisiae (yeast) |
| Journal | J Cell Biol |
| Year | 2000 |
| Peer reviewed | Yes |
| Record last updated | 2026-09-23 |
| Source | DOI 10.1083/jcb.150.6.1507 · PMID 10995454 |