Tor-mediated induction of autophagy via an Apg1 protein kinase complex

Citation
Y. Kamada et al., Tor-mediated induction of autophagy via an Apg1 protein kinase complex, J CELL BIOL, 150(6), 2000, pp. 1507-1513
Citations number
27
Categorie Soggetti
Cell & Developmental Biology
Journal title
JOURNAL OF CELL BIOLOGY
ISSN journal
00219525 → ACNP
Volume
150
Issue
6
Year of publication
2000
Pages
1507 - 1513
Database
ISI
SICI code
0021-9525(20000918)150:6<1507:TIOAVA>2.0.ZU;2-G
Abstract
Autophagy is a membrane trafficking to vacuole/lysosome induced by nutrient starvation. In Saccharomyces cerevisiae, Tor protein, a phosphatidylinosit ol kinase-related kinase, is involved in the repression of autophagy induct ion by a largely unknown mechanism, Here, we show that the protein kinase a ctivity of Apg1 is enhanced by starvation or rapamycin treatment. In additi on, we have also found that Apg13, which binds to and activates Apg1, is hy perphosphorylated in a Tor-dependent manner, reducing its affinity to Apg1. This Apg1-Apg13 association is required for autophagy, but not for the cyt oplasm-to-vacuole targeting (Cvt) pathway, another vesicular transport mech anism in which factors essential for autophagy (Apg proteins) are also empl oyed under vegetative growth conditions. Finally, other Apg1-associating pr oteins, such as Apg17 and Cvt9, are shown to function specifically in autop hagy or the Cvt pathway, respectively, suggesting that the Apg1 complex pla ys an important role in switching between two distinct vesicular transport systems in a nutrient-dependent manner.