- 첨부된 파일이 없습니다.
- 담당교수Seung-Yeol Park
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.