期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 292, 期 20, 页码 8533-8543出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M116.762963
关键词
-
资金
- Ministry of Education, Culture, Sports, Science and Technology of Japan [23000015, 16H06375]
- Japan Society for the Promotion of Science
- Grants-in-Aid for Scientific Research [13J40059, 23000015, 16H06375] Funding Source: KAKEN
Autophagy is a bulk degradation process conserved from yeast to mammals. To examine the roles of autophagy in cellular metabolism, we generated autophagy-defective (atg) mutants in the X2180-1B strain background. We compared the growth of wild-type (WT) and atg cells in minimal (synthetic dextrose, SD) and rich (yeast extract/peptone/dextrose, YEPD) medium, and we found that mutations in the core autophagy machinery result in defects in the diauxic shift, the transition from fermentation to respiratory growth upon glucose depletion, specifically in SD. Furthermore, we confirmed that autophagy was induced prior to the diauxic shift, implying that it plays a role in this process. In YEPD, atg mutants grew normally, so we assumed that the insufficiency of certain nutrients in SD was responsible for the defects. We ultimately identified iron, which is a necessary cofactor for respiratory activity, as the nutrient required for the diauxic shift in atg mutants. Indeed, atg mutants exhibited defects in respiration, which was rescued by supplementation with iron. Based on these data, we hypothesized that autophagy is involved in iron recycling during the diauxic shift. smf3 Delta fet5 Delta or smf3 Delta ftr1 Delta cells, which are unable to export iron from the vacuole, also exhibit defects in the diauxic shift, so iron released from the vacuole is important for the shift in SD medium. Finally, we observed that smf3 Delta fet5 Delta cells accumulated nearly twice as much vacuolar iron as smf3 Delta fet5 Delta atg2 Delta cells, suggesting that autophagy is involved in iron recycling by the vacuolar transport and degradation of iron-containing cargos.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据