JCB logo
Epitomics: The Rabbit Monoclonal Company
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

Published online 18 September 2000. doi:10.1083/jcb.150.6.1507
This Article
Right arrow Full Text
Right arrow PDF (Full Text)
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kamada, Y.
Right arrow Articles by Ohsumi, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kamada, Y.
Right arrow Articles by Ohsumi, Y.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
© The Rockefeller University Press, 0021-9525/2000/9/1507/ $5.00
The Journal of Cell Biology, Volume 150, Number 6, September 18, 2000 1507-1513


Report

Tor-mediated Induction of Autophagy Via an Apg1 Protein Kinase Complex

Yoshiaki Kamadaa,b, Tomoko Funakoshia, Takahiro Shintania, Kazuya Naganoc, Mariko Ohsumic, and Yoshinori Ohsumia,b
a Department of Cell Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan
b School of Life Science, The Graduate University for Advanced Studies, Okazaki 444-8585, Japan
c Department of Biosciences, Teikyo University of Science and Technology, Yamanashi 409-0193, Japan

Correspondence to: Yoshinori Ohsumi, Department of Cell Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan. Tel:81-564-55-7515 Fax:81-564-55-7516

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. This Apg1–Apg13 association is required for autophagy, but not for the cytoplasm-to-vacuole targeting (Cvt) pathway, another vesicular transport mechanism in which factors essential for autophagy (Apg proteins) are also employed under vegetative growth conditions. Finally, other Apg1-associating proteins, such as Apg17 and Cvt9, are shown to function specifically in autophagy or the Cvt pathway, respectively, suggesting that the Apg1 complex plays an important role in switching between two distinct vesicular transport systems in a nutrient-dependent manner.

Key Words: starvation, Cvt, yeast, rapamycin, phosphorylation


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents