A role for TOR complex 2 signaling in promoting autophagy

Ariadne Vlahakis, Ted Powers

Research output: Contribution to journalArticle

21 Scopus citations

Abstract

The conserved target of rapamycin (TOR) kinase is a central regulator of cell growth in response to nutrient availability. TOR forms 2 structurally and functionally distinct complexes, TORC1 and TORC2, and negatively regulates autophagy via TORC1. Here we demonstrate TOR also operates independently through the TORC2 signaling pathway to promote autophagy upon amino acid limitation. Under these conditions, TORC2, through its downstream target kinase Ypk1, inhibits the Ca2+ and Cmd1/calmodulin-dependent phosphatase, calcineurin, to enable the activation of the amino acid-sensing EIF2S1/eIF2α kinase, Gcn2, and promote autophagy. Thus TORC2 signaling regulates autophagy in a pathway distinct from TORC1 to provide a tunable response to the cellular metabolic state.

Original languageEnglish (US)
Pages (from-to)2085-2086
Number of pages2
JournalAutophagy
Volume10
Issue number11
DOIs
StatePublished - Nov 1 2014

Keywords

  • Amino acid
  • Calcineurin
  • GAAC
  • Gcn2
  • Gcn4
  • Nitrogen
  • TOR
  • TORC1
  • TORC2
  • Ypk1

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology

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