MON-2, a Golgi protein, mediates autophagy-dependent longevity in Caenorhabditis elegans
| Autor: | Dongyeop Lee, Hyun-Jun Nam, Chanhee Kang, Jooyeon Sohn, Malene Hansen, Linnea M Adams, Yujin Lee, Eun Ji Kim, Seung-Yeol Park, Murat Artan, Dae-Eun Jeong, Dong Jin Moon, Wooseon Hwang, Seung-Jae Lee, Joo-Yeon Yoo, Mihwa Seo, Jeonghun Yeom, Yoonji Jung, Ozlem Altintas, Youngjae Ryu, Sang Ki Park, Cheolju Lee, Keunhee Seo, Sanguk Kim, Chang Man Ha, Seong Kyu Han, Nari Kim, Ara B. Hwang, Sungeun Ju |
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| Rok vydání: | 2021 |
| Předmět: | |
| Zdroj: | Science Advances |
| ISSN: | 2375-2548 |
| Popis: | Description MON-2, which mediates Golgi-endosome trafficking, mediates mitochondrial inhibition–induced longevity by enhancing autophagy. The Golgi apparatus plays a central role in trafficking cargoes such as proteins and lipids. Defects in the Golgi apparatus lead to various diseases, but its role in organismal longevity is largely unknown. Using a quantitative proteomic approach, we found that a Golgi protein, MON-2, was up-regulated in long-lived Caenorhabditis elegans mutants with mitochondrial respiration defects and was required for their longevity. Similarly, we showed that DOP1/PAD-1, which acts with MON-2 to traffic macromolecules between the Golgi and endosome, contributed to the longevity of respiration mutants. Furthermore, we demonstrated that MON-2 was required for up-regulation of autophagy, a longevity-associated recycling process, by activating the Atg8 ortholog GABARAP/LGG-1 in C. elegans. Consistently, we showed that mammalian MON2 activated GABARAPL2 through physical interaction, which increased autophagic flux in mammalian cells. Thus, the evolutionarily conserved role of MON2 in trafficking between the Golgi and endosome is an integral part of autophagy-mediated longevity. |
| Databáze: | OpenAIRE |
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