期刊
AUTOPHAGY
卷 7, 期 1, 页码 17-26出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/auto.7.1.13840
关键词
autophagy; DFCP1; Rab1; Salmonella; ER-to-golgi trafficking
类别
资金
- Burroughs Wellcome Fund
- Canadian Foundation for Innovation
- Ontario Innovation Trust
- Natural Sciences and Engineering Research Council of Canada
- Canadian Association of Gastroenterology (CAG)/Canadian Institutes of Health Research/Crohn's and Colitis Foundation of Canada
- Biotechnology and Biological Sciences Research Council [BBS/E/B/00001221] Funding Source: researchfish
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI074760] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM053396, R01GM059609] Funding Source: NIH RePORTER
Autophagy mediates the degradation of cytoplasmic components in eukaryotic cells and plays a key role in immunity. The mechanism of autophagosome formation is not clear. Here we examined two potential membrane sources for antibacterial autophagy: the ER and mitochondria. DFCP1, a marker of specialized ER domains known as 'omegasomes,' associated with Salmonella-containing autophagosomes via its PtdIns(3)P and ER-binding domains, while a mitochondrial marker (cytochrome b5-GFP) did not. Rab1 also localized to autophagosomes, and its activity was required for autophagosome formation, clearance of protein aggregates and peroxisomes, and autophagy of Salmonella. Overexpression of Rab1 enhanced antibacterial autophagy. The role of Rab1 in antibacterial autophagy was independent of its role in ER-to-Golgi transport. Our data suggest that antibacterial autophagy occurs at omegasomes and reveal that the Rab1 GTPase plays a crucial role in mammalian autophagy.
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