The extracytoplasmic function sigma factor σVreI is active during infection and contributes to phosphate starvation-induced virulence of Pseudomonas aeruginosa
Joaquín R. Otero‐Asman, José Miguel Quesada, Kin Ki Jim, Alain A. Ocampo-Sosa, Cristina Civantos, Wilbert Bitter, María A. Llamas
Abstract
Abstract The extracytoplasmic function sigma factor σ VreI 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 σ VreI 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 σ VreI 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 σ VreI is active during infection and that lack of σ VreI considerably reduces the Pi starvation-induced virulence of this pathogen. Surprisingly, lack of the σ VreI 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 σ VreI -dependent but also in a σ VreI -independent manner. This includes potential virulence determinants and transcriptional regulators that could be responsible for the reduced virulence of the ΔvreR mutant.