Dissemin is shutting down on January 1st, 2025

Published in

American Society for Cell Biology, Molecular Biology of the Cell, 4(25), p. 522-531

DOI: 10.1091/mbc.e13-10-0574

Links

Tools

Export citation

Search in Google Scholar

Rab11 facilitates cross-talk between autophagy and endosomal pathway through regulation of Hook localization

Journal article published in 2013 by Zsuzsanna Szatmári, Pé ter Lorincz, Viktor Kis, Mónika Lippai, Krisztina Hegedus, Tamás Faragó, Péter Lorincz ORCID, Tsubasa Tanaka, Gábor Juhász ORCID, Miklós Sass
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

Full text: Download

Red circle
Preprint: archiving forbidden
Green circle
Postprint: archiving allowed
Upload
Orange circle
Published version: archiving restricted
Upload
Policy details
Data provided by SHERPA/RoMEO

Abstract

During autophagy, double-membrane autophagosomes deliver sequestered cytoplasmic content to late endosomes and lysosomes for degradation. The molecular mechanism of autophagosome maturation is still poorly characterized. The small GTPase Rab11 regulates endosomal traffic, and is thought to function at the level of recycling endosomes. Here we show that loss of Rab11 leads to accumulation of autophagosomes and late endosomes in Drosophila melanogaster. Rab11 translocates from recycling endosomes to autophagosomes in response to autophagy induction, and physically interacts with Hook, a negative regulator of endosome maturation. Hook anchors endosomes to microtubules, and we show that Rab11 facilitates the fusion of endosomes and autophagosomes by removing Hook from mature late endosomes and inhibiting its homodimerization. Thus, induction of autophagy appears to promote autophagic flux by increased convergence with the endosomal pathway.