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Mucosal penetration primes Vibrio cholerae for host colonization by repressing quorum sensing
Zhi Liu1, Tim Miyashiro, Amy Tsou
1Departments of Microbiology, Physics, and Biology, University of Pennsylvania, Philadelphia, PA 19104, USA.
Summary
Vibrio cholerae uses its flagellar machinery to regulate virulence gene expression. FliA represses hapR, a key regulator, impacting cholera pathogenesis and colonization.
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Gene Regulation
Background:
- Vibrio cholerae causes cholera by invading the intestinal lining and expressing virulence factors.
- The quorum sensing regulator HapR normally represses virulence gene expression in V. cholerae.
- Understanding V. cholerae colonization mechanisms is crucial for developing effective interventions.
Purpose of the Study:
- To investigate the role of flagellar assembly in regulating HapR expression and virulence in V. cholerae.
- To elucidate the interaction between the FliA regulatory network and HapR during host colonization.
Main Methods:
- Analysis of hapR gene expression in wild-type and mutant V. cholerae strains.
- Assessment of flagellar integrity and FlgM secretion during host cell interaction.
- Evaluation of bacterial colonization in a host model.
Main Results:
- FliA, an alternative sigma factor, directly represses hapR expression.
- Flagellar breakage upon mucin penetration releases the anti-sigma factor FlgM, which inhibits FliA.
- fliA mutants exhibit reduced hapR repression and attenuated intestinal colonization.
Conclusions:
- V. cholerae utilizes flagellar components to sense intestinal cues and modulate virulence.
- The FliA-FlgM-HapR regulatory axis plays a critical role in V. cholerae pathogenesis.
- Targeting this pathway could offer novel strategies for controlling cholera.
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