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Stringent response interacts with the ToxR regulon to regulate Vibrio cholerae virulence factor expression
David M Raskin1, Arunima Mishra2,3, Huajun He2
1College of Osteopathic Medicine, Marian University, 3200 Cold Spring Road, Indianapolis, IN, 46222-1997, USA. draskin@marian.edu.
Archives of Microbiology
|March 12, 2020
Summary
The stringent response is crucial for Vibrio cholerae to colonize the gut and express virulence factors like toxin-coregulated pilus (TCP). This stress response regulates the ToxR regulon, impacting cholera
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Molecular Biology
Background:
- Cholera is a diarrheal disease caused by Vibrio cholerae.
- Virulence factors, including toxin-coregulated pilus (TCP) and cholera toxin, are essential for V. cholerae infection.
- Gene expression is regulated by the ToxR regulon, involving ToxR, TcpP, and ToxT.
Purpose of the Study:
- To investigate the role of the stringent response in regulating V. cholerae virulence genes.
- To determine if the stringent response influences TCP and cholera toxin expression.
- To elucidate the mechanism by which stringent response affects the ToxR regulon.
Main Methods:
- Utilized an infant mouse model to assess V. cholerae colonization.
- Created and analyzed V. cholerae strains with deletions in stringent response genes.
- Measured expression levels of virulence genes (toxT, tcpPH, toxRS) under stringent response conditions.
Main Results:
- V. cholerae strains lacking stringent response genes failed to colonize the infant mouse small intestine.
- Stringent response was essential for TCP expression but had non-significant effects on cholera toxin expression.
- Stringent response induced toxT and tcpPH expression while repressing toxRS.
Conclusions:
- The stringent response is a critical regulator of V. cholerae virulence.
- Stringent response controls TCP and cholera toxin expression through differential regulation of the ToxR regulon components.
- Understanding this regulation provides insights into cholera pathogenesis.
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