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Updated: Dec 28, 2025

A Fluorescence-based Method to Study Bacterial Gene Regulation in Infected Tissues
Published on: February 19, 2019
The extracytoplasmic function sigma factor σVreI is active during infection and contributes to phosphate
Joaquín R Otero-Asman1, José M Quesada1, Kin K Jim2
1Department of Environmental Protection, Estación Experimental del Zaidín-Consejo Superior de Investigaciones Científicas, Granada, Spain.
Abstract:
The extracytoplasmic function sigma factor σVreI of the human pathogen Pseudomonas aeruginosa promotes transcription of potential virulence determinants, including secretion systems and secreted proteins. Its activity is modulated by the VreR anti-σ factor that inhibits the binding of σVreI to the RNA polymerase in the absence of a (still unknown) inducing signal. The vreI-vreR genes are expressed under inorganic phosphate (Pi) starvation, a physiological condition often encountered in the host that increases P. aeruginosa pathogenicity. However, whether or not σVreI is active in vivo during infection and contributes to the Pi starvation-induced virulence of this pathogen has not been analyzed yet. Using zebrafish embryos and a human alveolar basal epithelial cell line as P. aeruginosa hosts, we demonstrate in this work that σVreI is active during infection and that lack of σVreI considerably reduces the Pi starvation-induced virulence of this pathogen. Surprisingly, lack of the σVreI inhibitor, the VreR anti-σ factor, also diminishes the virulence of P. aeruginosa. By transcriptomic analyses we show that VreR modulates gene expression not only in a σVreI-dependent but also in a σVreI-independent manner. This includes potential virulence determinants and transcriptional regulators that could be responsible for the reduced virulence of the ΔvreR mutant.
Insights
The sigma factor VreI is active during Pseudomonas aeruginosa infection, contributing to virulence under phosphate starvation. Surprisingly, its inhibitor VreR also impacts virulence, suggesting complex regulatory roles.
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Molecular Biology
Background:
- The extracytoplasmic function sigma factor σVreI in Pseudomonas aeruginosa regulates virulence factors.
- σVreI activity is controlled by the anti-σ factor VreR, particularly under inorganic phosphate (Pi) starvation.
- The role of σVreI in vivo during infection and its contribution to Pi starvation-induced virulence remain uncharacterized.
Purpose of the Study:
- To investigate the in vivo activity and role of σVreI during Pseudomonas aeruginosa infection.
- To determine the contribution of σVreI to Pi starvation-induced virulence.
- To elucidate the function of the VreR anti-σ factor in P. aeruginosa pathogenicity.
Main Methods:
- Utilized zebrafish embryos and a human alveolar basal epithelial cell line as infection models.
- Assessed the virulence of wild-type, ΔvreI, and ΔvreR P. aeruginosa mutants.
- Performed transcriptomic analyses to understand gene expression changes.
Main Results:
- σVreI is active during P. aeruginosa infection and is crucial for Pi starvation-induced virulence.
- Deletion of the VreR anti-σ factor also reduced P. aeruginosa virulence.
- VreR influences gene expression both dependently and independently of σVreI, affecting virulence determinants and regulators.
Conclusions:
- σVreI plays a significant role in P. aeruginosa virulence during infection, especially under Pi-limiting conditions.
- The anti-σ factor VreR has a complex regulatory role, impacting virulence through both σVreI-dependent and -independent pathways.
- Further investigation into VreR's targets is needed to fully understand its contribution to P. aeruginosa pathogenicity.
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