Susceptibility of Toxoplasma gondii to autophagy in human cells relies on multiple interacting parasite loci.
| Autor: | Rinkenberger N; Department of Molecular Microbiology, Washington University School of Medicine, St Louis, Missouri, USA., Rosenberg A; Department of Molecular Microbiology, Washington University School of Medicine, St Louis, Missouri, USA., Radke JB; Department of Molecular Microbiology, Washington University School of Medicine, St Louis, Missouri, USA., Bhushan J; Department of Molecular Microbiology, Washington University School of Medicine, St Louis, Missouri, USA., Tomita T; Department of Pathology, Albert Einstein College of Medicine, Bronx, New York, USA., Weiss LM; Department of Pathology, Albert Einstein College of Medicine, Bronx, New York, USA.; Department of Medicine, Albert Einstein College of Medicine, Bronx, New York, USA., Sibley LD; Department of Molecular Microbiology, Washington University School of Medicine, St Louis, Missouri, USA. |
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| Jazyk: | angličtina |
| Zdroj: | MBio [mBio] 2024 Jan 16; Vol. 15 (1), pp. e0259523. Date of Electronic Publication: 2023 Dec 14. |
| DOI: | 10.1128/mbio.02595-23 |
| Abstrakt: | Importance: Autophagy is a process used by cells to recycle organelles and macromolecules and to eliminate intracellular pathogens. Previous studies have shown that some stains of Toxoplasma gondii are resistant to autophagy-dependent growth restriction, while others are highly susceptible. Although it is known that autophagy-mediated control requires activation by interferon gamma, the basis for why parasite strains differ in their susceptibility is unknown. Our findings indicate that susceptibility involves at least five unlinked parasite genes on different chromosomes, including several secretory proteins targeted to the parasite-containing vacuole and exposed to the host cell cytosol. Our findings reveal that susceptibility to autophagy-mediated growth restriction relies on differential recognition of parasite proteins exposed at the host-pathogen interface, thus identifying a new mechanism for cell-autonomous control of intracellular pathogens. Competing Interests: The authors declare no conflict of interest. |
| Databáze: | MEDLINE |
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