Selective Subversion of Autophagy Complexes Facilitates Completion of the Brucella Intracellular Cycle

Tregei Starr; Robert Child; Tara D Wehrly; Bryan Hansen; Seungmin Hwang; Carlos López-Otin; Herbert W Virgin; Jean Celli

doi:10.1016/j.chom.2011.12.002

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Selective Subversion of Autophagy Complexes Facilitates Completion of the Brucella Intracellular Cycle

Journal article

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Selective Subversion of Autophagy Complexes Facilitates Completion of the Brucella Intracellular Cycle

Tregei Starr, Robert Child, Tara D Wehrly, Bryan Hansen, Seungmin Hwang, Carlos López-Otin, Herbert W Virgin and Jean Celli

Cell host & microbe, Vol.11(1), pp.33-45

2012

DOI: https://doi.org/10.1016/j.chom.2011.12.002

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https://hdl.handle.net/2376/114448

PMCID: PMC3266535

PMID: 22264511

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https://doi.org/10.1016/j.chom.2011.12.002View

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Abstract

Autophagy is a cellular degradation process that can capture and eliminate intracellular microbes by delivering them to lysosomes for destruction. However, pathogens have evolved mechanisms to subvert this process. The intracellular bacterium Brucella abortus ensures its survival by forming the Brucella-containing vacuole (BCV), which traffics from the endocytic compartment to the endoplasmic reticulum (ER), where the bacterium proliferates. We show that Brucella replication in the ER is followed by BCV conversion into a compartment with autophagic features (aBCV). While Brucella trafficking to the ER was unaffected in autophagy-deficient cells, aBCV formation required the autophagy-initiation proteins ULK1, Beclin 1, and ATG14L and PI3-kinase activity. However, aBCV formation was independent of the autophagy-elongation proteins ATG5, ATG16L1, ATG4B, ATG7, and LC3B. Furthermore, aBCVs were required to complete the intracellular Brucella lifecycle and for cell-to-cell spreading, demonstrating that Brucella selectively co-opts autophagy-initiation complexes to subvert host clearance and promote infection. ► Brucella translocates to endosomal vacuoles following replication in the ER ► Brucella selectively co-opts proteins involved in autophagosome nucleation ► Subversion of autophagy by Brucella promotes completion of its infection cycle

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Title: Selective Subversion of Autophagy Complexes Facilitates Completion of the Brucella Intracellular Cycle
Creators: Tregei Starr - Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA
Robert Child - Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA
Tara D Wehrly - Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA
Bryan Hansen - Electron Microscopy Unit, Research Technologies Branch, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA
Seungmin Hwang - Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA
Carlos López-Otin - Departamento de Bioquímica y Biología Molecular, Facultad de Medicina, Instituto Universitario de Oncología, Universidad de Oviedo, 33006 Oviedo, Spain
Herbert W Virgin - Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA
Jean Celli - Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA
Publication Details: Cell host & microbe, Vol.11(1), pp.33-45
Academic Unit: Paul G. Allen School for Global Animal Health
Publisher: Elsevier Inc
Identifiers: 99900547307001842
Language: English
Resource Type: Journal article