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Vibrio cholerae requires rpoS for efficient intestinal colonization.
D S Merrell1, A D Tischler, S H Lee
1Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
Infection and Immunity
|November 18, 2000
Summary
The alternative sigma factor RpoS is crucial for Vibrio cholerae intestinal colonization in mice. Mutations in rpoS significantly reduced colonization, highlighting RpoS
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Molecular Biology
Background:
- Vibrio cholerae is an intestinal pathogen found in aquatic environments.
- Vibrio cholerae causes diarrheal disease through intestinal colonization in animal models.
- The role of specific regulatory factors in V. cholerae colonization is not fully understood.
Purpose of the Study:
- To investigate the role of the alternative sigma factor RpoS in Vibrio cholerae intestinal colonization.
- To determine if RpoS is essential for V. cholerae pathogenesis in a suckling mouse model.
Main Methods:
- Construction of independent mutations within the rpoS gene.
- Assessment of V. cholerae colonization ability using competition assays in suckling mice.
- Evaluation of in vitro growth characteristics of mutant strains.
- Analysis of spontaneous suppressor mutations.
- Complementation of mutant phenotypes through trans-acting rpoS expression or allelic reversion.
Main Results:
- Multiple independent rpoS mutations resulted in a fivefold decrease in V. cholerae intestinal colonization.
- rpoS mutations did not affect in vitro growth in rich medium.
- Spontaneous suppressor mutations were ruled out as a confounding factor.
- Complementation studies confirmed that the reduced colonization was due to loss of functional RpoS.
Conclusions:
- The alternative sigma factor RpoS plays a significant role in Vibrio cholerae intestinal colonization.
- RpoS is essential for the colonization fitness of V. cholerae in the suckling mouse model.
- These findings identify RpoS as a key factor in V. cholerae pathogenesis.