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.
Abstract
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Autophagy is a membrane trafficking to vacuole/lysosome induced by nutrient starvation. In Saccharomyces cerevisiae, Tor protein, a phosphatidylinositol kinase-related kinase, is involved in the repression of autophagy induction by a largely unknown mechanism. Here, we show that the protein kinase activity of Apg1 is enhanced by starvation or rapamycin treatment. In addition, we have also found that Apg13, which binds to and activates Apg1, is hyperphosphorylated in a Tor-dependent manner, reducing its affinity to Apg1.
Read the full abstract on PubMed →At a glance
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| 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 | Journal of Cell Biology |
| Year | 2000 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1083/jcb.150.6.1507 · PMID 10995454 |
Where this study fits
How this study connects to the pathway map, open questions, people and other studies in the Atlas.
People in the Atlas
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Showed as first author that TOR keeps autophagy switched off in yeast by controlling the Atg1 (Apg1) kinase complex, and has studied TOR's control of autophagy ever since
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Found the genes that make autophagy work, and with them the link from TOR to the autophagy machinery
More: 4 other authors
No profile yet: Funakoshi T, Shintani T, Nagano K, Ohsumi M
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Topics
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | Nitrogen starvation; rapamycin |
| Target | Tor - Apg13 - Apg1 (ULK1 orthologue) kinase complex |
| Model | Saccharomyces cerevisiae |
| Effect | Tor keeps Apg13 hyperphosphorylated, preventing Apg1 activation; starvation or rapamycin raises Apg1 kinase activity and induces autophagy. |
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