Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/99959
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Type: Journal article
Title: Atg9 is required for intraluminal vesicles in amphisomes and autolysosomes
Author: Bader, C.
Shandala, T.
Ng, Y.
Johnson, I.
Brooks, D.
Citation: Biology Open, 2015; 4(11):1345-1355
Publisher: Company of Biologists
Issue Date: 2015
ISSN: 2046-6390
2046-6390
Statement of
Responsibility: 
C. A. Bader, T. Shandala, Y. S. Ng, I. R. D. Johnson, D. A. Brooks
Abstract: Autophagy is an intracellular recycling and degradation process, which is important for energy metabolism, lipid metabolism, physiological stress response and organism development. During Drosophila development, autophagy is up-regulated in fat body and midgut cells, to control metabolic function and to enable tissue remodelling. Atg9 is the only transmembrane protein involved in the core autophagy machinery and is thought to have a role in autophagosome formation. During Drosophila development, Atg9 co-located with Atg8 autophagosomes, Rab11 endosomes and Lamp1 endosomes-lysosomes. RNAi silencing of Atg9 reduced both the number and the size of autophagosomes during development and caused morphological changes to amphisomes/autolysosomes. In control cells there was compartmentalised acidification corresponding to intraluminal Rab11/Lamp-1 vesicles, but in Atg9 depleted cells there were no intraluminal vesicles and the acidification was not compartmentalised. We concluded that Atg9 is required to form intraluminal vesicles and for localised acidification within amphisomes/autolysosomes, and consequently when depleted, reduced the capacity to degrade and remodel gut tissue during development.
Keywords: Atg9; autophagy; autophagosome; amphisome; autolysosome; multivesicular endosome; lysosome; intraluminal vesicles
Rights: © 2015. Published by The Company of Biologists Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.
RMID: 0030038388
DOI: 10.1242/bio.013979
Grant ID: http://purl.org/au-research/grants/nhmrc/631915
Appears in Collections:Molecular and Biomedical Science publications

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