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Cited 6 time in webofscience Cited 6 time in scopus
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MON-2, a Golgi protein, mediates autophagy-dependent longevity in Caenorhabditis elegans

Authors
Jung, YoonjiArtan, MuratKim, NariYeom, JeonghunHwang, Ara B.Jeong, Dae-EunAltintas, OzlemSeo, KeunheeSeo, MihwaLee, DongyeopHwang, WooseonLee, YujinSohn, JooyeonKim, Eun Ji E.Ju, SungeunHan, Seong KyuNam, Hyun-JunAdams, LinneaRyu, YoungjaeMoon, Dong JinKang, ChanheeYoo, Joo-YeonPark, Sang KiHa, Chang ManHansen, MaleneKim, SangukLee, CheoljuPark, Seung-YeolLee, Seung-Jae, V
Issue Date
Dec-2021
Publisher
AMER ASSOC ADVANCEMENT SCIENCE
Citation
SCIENCE ADVANCES, v.7, no.49
Journal Title
SCIENCE ADVANCES
Volume
7
Number
49
URI
http://scholarworks.bwise.kr/kbri/handle/2023.sw.kbri/270
DOI
10.1126/sciadv.abj8156
ISSN
2375-2548
Abstract
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.
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