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Updated: Jul 2, 2025

Immunofluorescence Analysis of Stress Granule Formation After Bacterial Challenge of Mammalian Cells
Published on: July 3, 2017
Shigella induces stress granule formation by ADP-riboxanation of the eIF3 complex
Qinxin Zhang1, Wei Xian1, Zilin Li2
1Department of Microbiology and Infectious Disease Center, NHC Key Laboratory of Medical Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China.
Abstract:
Under stress conditions, translationally stalled mRNA and associated proteins undergo liquid-liquid phase separation and condense into cytoplasmic foci called stress granules (SGs). Many viruses hijack SGs for their pathogenesis; however, whether pathogenic bacteria also exploit this pathway remains unknown. Here, we report that members of the OspC family of Shigella flexneri induce SG formation in infected cells. Mechanistically, the OspC effectors target multiple subunits of the host translation initiation factor 3 complex by ADP-riboxanation. The modification of eIF3 leads to translational arrest and thus the formation of SGs. Furthermore, OspC-mediated SGs are beneficial for S. flexneri replication within infected host cells, and bacterial strains unable to induce SGs are attenuated for virulence in a murine model of infection. Our findings reveal a mechanism by which bacterial pathogens induce SG assembly by inactivating host translational machinery and promote bacterial proliferation in host cells.
Insights
Pathogenic bacteria, Shigella flexneri, exploit host stress granules (SGs) by targeting translation factors. This SG formation aids bacterial replication and virulence, revealing a novel pathogenic mechanism.
Area of Science:
- Cellular Biology
- Microbiology
- Pathogenesis
Background:
- Stress granules (SGs) are cytoplasmic foci formed from translationally stalled mRNA and proteins under stress.
- Viruses are known to hijack SGs for pathogenesis.
- The role of SGs in bacterial pathogenesis was previously unknown.
Purpose of the Study:
- To investigate whether pathogenic bacteria exploit stress granules for their benefit.
- To elucidate the mechanism by which bacteria induce SG formation.
- To determine the role of SG formation in bacterial virulence and replication.
Main Methods:
- Studying Shigella flexneri infection models.
- Analyzing the interaction of OspC effectors with host translation initiation factor 3 (eIF3).
- Utilizing murine models of infection to assess bacterial virulence.
Main Results:
- Shigella flexneri OspC proteins induce stress granule formation in infected host cells.
- OspC effectors ADP-riboxylate eIF3 subunits, leading to translational arrest and SG assembly.
- SG formation is beneficial for S. flexneri replication and bacterial strains lacking this ability are attenuated in virulence.
Conclusions:
- Bacterial pathogens can induce SG assembly by inactivating host translational machinery.
- Stress granules serve as a platform that promotes bacterial proliferation within host cells.
- This study reveals a novel mechanism of bacterial pathogenesis involving host stress granules.
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