MON-2, a Golgi protein, promotes longevity by upregulating autophagy through mediating inter-organelle communications

The Golgi apparatus regulates the process of modification and subcellular localization of macromolecules, including proteins and lipids. Aberrant protein sorting caused by defects in the Golgi leads to various diseases in mammals. However, the role of the Golgi apparatus in organismal longevity rema...

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Bibliographic Details
Published in:Autophagy 2022-05, Vol.18 (5), p.1208-1210
Main Authors: Artan, Murat, Sohn, Jooyeon, Lee, Cheolju, Park, Seung-Yeol, Lee, Seung-Jae V.
Format: Article
Language:English
Subjects:
Aging
Animals
Autophagic Punctum
autophagy
Autophagy - physiology
C. elegans
Caenorhabditis elegans
Endosomes - metabolism
Golgi
Golgi Apparatus - metabolism
LGG-1/GABARAPL2
lifespan
Longevity
Mammals
MON-2/MON2
Proteomics
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Summary:The Golgi apparatus regulates the process of modification and subcellular localization of macromolecules, including proteins and lipids. Aberrant protein sorting caused by defects in the Golgi leads to various diseases in mammals. However, the role of the Golgi apparatus in organismal longevity remained largely unknown. By employing a quantitative proteomic approach, we demonstrated that MON-2, an evolutionarily conserved Arf-GEF protein implicated in Golgi-to-endosome trafficking, promotes longevity via upregulating macroautophagy/autophagy in C. elegans. Our data using cultured mammalian cells indicate that MON2 translocates from the Golgi to the endosome under starvation conditions, subsequently increasing autophagic flux by binding LGG-1/GABARAPL2. Thus, Golgi-to-endosome trafficking appears to be an evolutionarily conserved process for the upregulation of autophagy, which contributes to organismal longevity.
ISSN:1554-8627
1554-8635
DOI:10.1080/15548627.2022.2039523