Loss of drosophila Vps16A enhances autophagosome formation through reduced Tor activity

Szabolcs Takáts, Ágnes Varga, Karolina Pircs, Gábor Juhász

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

The HOPS tethering complex facilitates autophagosome-lysosome fusion by binding to Syx17 (Syntaxin 17), the autophagosomal SNARE. Here we show that loss of the core HOPS complex subunit Vps16A enhances autophagosome formation and slows down Drosophila development. Mechanistically, Tor kinase is less active in Vps16A mutants likely due to impaired endocytic and biosynthetic transport to the lysosome, a site of its activation. Tor reactivation by overexpression of Rheb suppresses autophagosome formation and restores growth and developmental timing in these animals. Thus, Vps16A reduces autophagosome numbers both by indirectly restricting their formation rate and by directly promoting their clearance. In contrast, the loss of Syx17 blocks autophagic flux without affecting the induction step in Drosophila.

Original languageEnglish
Pages (from-to)1209-1215
Number of pages7
JournalAutophagy
Volume11
Issue number8
DOIs
Publication statusPublished - Jan 1 2015

Keywords

  • Autophagy
  • Flux
  • HOPS
  • Lysosome
  • Syntaxin 17
  • Tor
  • Vps16A

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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