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Loss of Drosophila Vps16A enhances autophagosome formation through reduced Tor activity.

Autophagy (2015-06-11)
Szabolcs Takáts, Ágnes Varga, Karolina Pircs, Gábor Juhász
ANOTACE

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.

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Sigma-Aldrich
Anti-Rabbit IgG (whole molecule)–Alkaline Phosphatase antibody produced in goat, affinity isolated antibody, buffered aqueous glycerol solution
Sigma-Aldrich
Goat Anti-Mouse IgG Antibody, Alkaline Phosphatase conjugate, Chemicon®, from goat