Loss of Drosophila Vps16A enhances autophagosome formation through reduced Tor activity

Research output: Contribution to journalArticle


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.


External organisations
  • Eötvös Loránd University
Research areas and keywords


  • Animals, Autophagy, Cloning, Molecular, Densitometry, Drosophila Proteins, Drosophila melanogaster, Endocytosis, Gene Expression Regulation, Developmental, Lipids, Lysosomes, Models, Genetic, Mutation, Phagosomes, Phosphorylation, Polymerase Chain Reaction, Qa-SNARE Proteins, Transcription Factors, Up-Regulation, Vesicular Transport Proteins, Journal Article, Research Support, Non-U.S. Gov't
Original languageEnglish
Pages (from-to)1209-15
Number of pages7
Issue number8
Publication statusPublished - 2015
Publication categoryResearch