Identification of Autophagy-Inhibiting Factors of Mycobacterium tuberculosis by High-Throughput Loss-of-Function Screening

Author:

Strong Emily J.1,Jurcic Smith Kristen L.2,Saini Neeraj K.3,Ng Tony W.3,Porcelli Steven A.34,Lee Sunhee125ORCID

Affiliation:

1. Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas, USA

2. Human Vaccine Institute, Duke University, Durham, North Carolina, USA

3. Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York, USA

4. Department of Medicine, Albert Einstein College of Medicine, Bronx, New York, USA

5. Department of Molecular Genetics and Microbiology, Duke University, Durham, North Carolina, USA

Abstract

The interaction of host cells with mycobacteria is complex and can lead to multiple outcomes ranging from bacterial clearance to progressive or latent infection. Autophagy is recognized as one component of host cell responses that has an essential role in innate and adaptive immunity to intracellular bacteria. Many microbes, including Mycobacterium tuberculosis , have evolved to evade or exploit autophagy, but the precise mechanisms and virulence factors are mostly unknown. Through a loss-of-function screening of an M. tuberculosis transposon mutant library, we identified 16 genes that contribute to autophagy inhibition, six of which encoded the PE/PPE protein family.

Funder

Division of Intramural Research, National Institute of Allergy and Infectious Diseases

Publisher

American Society for Microbiology

Subject

Infectious Diseases,Immunology,Microbiology,Parasitology

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