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Updated: Jun 13, 2026

Super-Resolution Imaging of Bacterial Secreted Proteins Using Genetic Code Expansion
Published on: February 10, 2023
pH sensing by intracellular Salmonella induces effector translocation
Xiu-Jun Yu1, Kieran McGourty, Mei Liu
1Section of Microbiology, Centre for Molecular Microbiology and Infection, Imperial College London, Armstrong Road, London SW7 2AZ, UK.
Salmonella enterica uses a type III secretion system (T3SS) to inject effector proteins. This study reveals that Salmonella senses host cell pH to regulate T3SS function and protein delivery.
Area of Science:
- Microbiology
- Cell Biology
- Bacterial Pathogenesis
Background:
- Salmonella enterica is a significant intracellular pathogen.
- It utilizes the Salmonella pathogenicity island 2 (SPI-2) type III secretion system (T3SS) to deliver effector proteins into host cells.
- T3SS assembly is linked to vacuole acidification, but effector secretion is impaired at low pH.
Purpose of the Study:
- To investigate the regulation of SPI-2 T3SS effector secretion in Salmonella.
- To elucidate the role of SPI-2-encoded proteins (SsaM, SpiC, SsaL) in secretion control.
- To determine how Salmonella senses and responds to host cell pH.
Main Methods:
- Bacterial culture at different pH conditions (pH 5.0 and 7.2).
- Analysis of SPI-2 T3SS protein complex stability (SsaM, SpiC, SsaL).
- Monitoring of effector protein secretion.
- Infection of host cells and assessment of effector translocation.
Main Results:
- Mutant strains lacking SsaM, SpiC, and SsaL complexes showed activated effector secretion at low pH.
- Wild-type Salmonella exposed to neutral pH (7.2) after low pH growth (5.0) led to complex dissociation, degradation, and effector secretion.
- Acidification of host cell cytosol prevented complex degradation and effector translocation in infected cells.
Conclusions:
- Intravacuolar Salmonella senses host cytosolic pH.
- Sensing host pH triggers the degradation of regulatory protein complexes (SsaM/SpiC/SsaL).
- This degradation is essential for effector translocation into host cells.
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