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PsaF Is a Membrane-Localized pH Sensor That Regulates psaA Expression in Yersinia pestis
Joshua D Quinn1, Eric H Weening1, Virginia L Miller1,2
1Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, North Carolina, USA.
Journal of Bacteriology
|June 1, 2021
Summary
Yersinia pestis uses PsaF as a pH sensor to control virulence by stabilizing PsaE, an essential regulator of PsaA production. This mechanism ensures appropriate gene expression in different host environments.
Area of Science:
- Microbiology
- Molecular Biology
- Pathogenesis
Background:
- Yersinia pestis causes bubonic plague and requires the pH 6 antigen (PsaA) for virulence.
- PsaA production is regulated by temperature and pH, with mechanisms for pH control being poorly understood.
- Previous studies suggested pH affects the stability of regulatory proteins PsaE and PsaF, rather than their translation.
Purpose of the Study:
- To investigate the pH-dependent posttranslational mechanisms regulating PsaE and PsaF stability.
- To elucidate the role of PsaF as a potential pH sensor.
- To understand how pH influences the stability of PsaE and its impact on PsaA expression.
Main Methods:
- Utilized antibodies against endogenous PsaE and PsaF to quantify protein levels under varying pH conditions.
- Analyzed histidine residues in the periplasmic domain of PsaF for pH sensing capabilities.
- Investigated the role of PsaF in PsaE stability and the potential involvement of regulated intramembrane proteolysis.
Main Results:
- PsaE and PsaF levels are distinctly regulated by a specific pH threshold.
- Histidine residues in PsaF suggest its function as a pH sensor.
- PsaF is crucial for PsaE stability; in its absence at neutral pH, PsaE undergoes proteolytic degradation.
Conclusions:
- Yersinia pestis employs PsaF as a pH sensor to regulate PsaA expression by controlling PsaE stability.
- This pH-sensing mechanism allows Y. pestis to adapt gene expression to different host environments.
- Understanding this regulation provides insights into bacterial virulence and host-pathogen interactions.
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