한빛사 논문
Yoonji Jung1,†, Murat Artan2,†, Nari Kim2,†, Jeonghun Yeom3,†, Ara B. Hwang2, Dae-Eun Jeong2, Özlem Altintas2, Keunhee Seo2, Mihwa Seo2, Dongyeop Lee2, Wooseon Hwang2, Yujin Lee1, Jooyeon Sohn1, Eun Ji E. Kim1, Sungeun Ju2, Seong Kyu Han2, Hyun-Jun Nam2, Linnea Adams4, Youngjae Ryu5, Dong Jin Moon2, Chanhee Kang6, Joo-Yeon Yoo2, Sang Ki Park2, Chang Man Ha5, Malene Hansen4, Sanguk Kim2, Cheolju Lee3,*, Seung-Yeol Park2,*, Seung-Jae V. Lee1,*
1Department of Biological Sciences, Korea Advanced Institute of Science and Technology, 291 Daehak-ro, Yuseong-gu, Daejeon 34141, South Korea. 2Department of Life Sciences, Pohang University of Science and Technology, 77 Cheongam-ro, Nam-gu, Pohang, Gyeongbuk 37673, South Korea. 3Center for Theragnosis, Korea Institute of Science and Technology, Seoul 02792, South Korea. 4Development, Aging, and Regeneration Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA. 5Research Division and Brain Research Core Facilities of Korea Brain Research Institute, Daegu 41068, South Korea. 6School of Biological Sciences, College of Natural Sciences, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul 08826, South Korea.
*Corresponding author.
†These authors contributed equally to this work
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.
논문정보
관련 링크
연구자 키워드
관련분야 논문보기