Journal
AUTOPHAGY
Volume 15, Issue 8, Pages 1465-1466Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2019.1609862
Keywords
ATL3; GABARAP; hereditary sensory and autonomic neuropathies type 1 (HSANI); reticulophagy receptors; selective autophagy
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Funding
- Beijing Natural Science Foundation [5161001]
- National Natural Science Foundation of China (NSFC) [31671392, 31871353]
- National Key Research and Development Program of China, Stem Cell and Translational Research [2016YFA0100501]
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The endoplasmic reticulum (ER) is the largest membranous organelle, and its turnover ensures cellular homeostasis. The selective macroautophagy/autophagy of the ER (reticulophagy) guarantees the balance of ER turnover. However, the mechanism and physiological relevance of reticulophagy is largely unknown. Recently, we identified ATL3 (atlastin GTPase 3), generally considered to mediate ER fusion, as a receptor for reticulophagy. ATL3 specifically interacts with the GABARAP subfamily proteins of the Atg8-family, and this association is crucial for ATL3's role as a receptor for reticulophagy. Moreover, 2 hereditary sensory and autonomic neuropathies type 1 (HSANI)-associated mutations of ATL3 (Tyr192Cys and Pro338Arg) impair ATL3's binding to GABARAP and function in reticulophagy. Therefore, we illuminate a new function of ATL3 in reticulophagy and the potential physiological relevance of reticulophagy in neurodegenerative diseases.
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