1. Biochemistry and Chemical Biology
  2. Computational and Systems Biology
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Snf1/AMPK promotes the formation of Kog1/Raptor-bodies to increase the activation threshold of TORC1 in budding yeast

  1. James E Hughes Hallett
  2. Xiangxia Luo
  3. Andrew P Capaldi  Is a corresponding author
  1. Department of Molecular and Cellular Biology, United States
  2. University of Arizona, United States
Research Article
  • Cited 39
  • Views 3,086
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Cite this article as: eLife 2015;4:e09181 doi: 10.7554/eLife.09181

Abstract

The target of rapamycin complex I (TORC1) regulates cell growth and metabolism in eukaryotes. Previous studies have shown that nitrogen and amino acid signals activate TORC1 via the small GTPases, Gtr1/2. However, little is known about the way that other nutrient signals are transmitted to TORC1. Here we report that glucose starvation triggers disassembly of TORC1, and movement of the key TORC1 component Kog1/Raptor to a single body near the edge of the vacuole. These events are driven by Snf1/AMPK-dependent phosphorylation of Kog1 at Ser 491/494 and two nearby prion-like motifs. Kog1-bodies then serve to increase the threshold for TORC1 activation in cells that have been starved for a significant period of time. Together, our data show that Kog1-bodies create hysteresis (memory) in the TORC1 pathway and help ensure that cells remain committed to a quiescent state under suboptimal conditions. We suggest that other protein bodies formed in starvation conditions have a similar function.

Article and author information

Author details

  1. James E Hughes Hallett

    Molecular and Cellular Biology, Department of Molecular and Cellular Biology, Tucson, United States
    Competing interests
    The authors declare that no competing interests exist.
  2. Xiangxia Luo

    Department of Molecular and Cellular Biology, University of Arizona, Tucson, United States
    Competing interests
    The authors declare that no competing interests exist.
  3. Andrew P Capaldi

    Department of Molecular and Cellular Biology, University of Arizona, Tucson, United States
    For correspondence
    capaldi@email.arizona.edu
    Competing interests
    The authors declare that no competing interests exist.

Reviewing Editor

  1. Kevin Struhl, Harvard Medical School, United States

Publication history

  1. Received: June 2, 2015
  2. Accepted: October 5, 2015
  3. Accepted Manuscript published: October 6, 2015 (version 1)
  4. Version of Record published: December 9, 2015 (version 2)

Copyright

© 2015, Hughes Hallett et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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