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Authors: Ju Huang, Cheryl L. Birmingham, Shahab Shahnazari, Jessica Shiu, Yiyu T. Zheng, Adam C. Smith, Kenneth G. Campellone, Won Do Heo, Samantha Gruenheid, Tobias Meyer, Matthew D. Welch, Nicholas T. Ktistakis, Peter K. Kim, Daniel J. Klionsky and John H. Brumell

Ju Huang

Cell Biology Program; Hospital for Sick Children; Toronto, ON CA

Cheryl L. Birmingham

Cell Biology Program; Hospital for Sick Children; Toronto, ON CA; Department of Molecular Genetics and Institute of Medical Science; University of Toronto; Toronto, ON CA

Shahab Shahnazari

Cell Biology Program; Hospital for Sick Children; Toronto, ON CA; Department of Molecular Genetics and Institute of Medical Science; University of Toronto; Toronto, ON CA

Jessica Shiu

Cell Biology Program; Hospital for Sick Children; Toronto, ON CA

Yiyu T. Zheng

Cell Biology Program; Hospital for Sick Children; Toronto, ON CA; Department of Molecular Genetics and Institute of Medical Science; University of Toronto; Toronto, ON CA

Adam C. Smith

Cell Biology Program; Hospital for Sick Children; Toronto, ON CA; Department of Molecular Genetics and Institute of Medical Science; University of Toronto; Toronto, ON CA

Kenneth G. Campellone

Department of Molecular & Cell Biology; University of California, Berkeley; Berkeley, CA USA

Won Do Heo

Department of Biological Sciences and KI for the BioCentury; Korea Advanced Institute of Science and Technology; Daejeon, Korea

Samantha Gruenheid

Department of Microbiology and Immunology; McGill University; Montreal, QC CA

Tobias Meyer

Chemical and Systems Biology; Stanford University Medical School; Stanford, CA USA

Matthew D. Welch

Department of Molecular & Cell Biology; University of California, Berkeley; Berkeley, CA USA

Nicholas T. Ktistakis

Signalling Programme; Babraham Institute; Babraham, Cambridge UK

Peter K. Kim

Cell Biology Program; Hospital for Sick Children; Toronto, ON CA; Department Biochemistry; University of Toronto; Toronto, ON CA

Daniel J. Klionsky

Life Sciences Institute and Department of Molecular, Cellular and Developmental Biology, and Department of Biological Chemistry; University of Michigan; Ann Arbor, MI USA

John H. Brumell

Corresponding author: john.brumell@sickkids.ca
Cell Biology Program; Hospital for Sick Children; Toronto, ON CA; Department of Molecular Genetics and Institute of Medical Science; University of Toronto; Toronto, ON CA; Institute of Medical Science; University of Toronto; Toronto, ON, CA

Abstract:
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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