PUBLICATION

The extracytoplasmic function sigma factor σVreI is active during infection and contributes to phosphate starvation-induced virulence of Pseudomonas aeruginosa

Authors
Otero-Asman, J.R., Quesada, J.M., Jim, K.K., Ocampo-Sosa, A., Civantos, C., Bitter, W., Llamas, M.A.
ID
ZDB-PUB-200225-15
Date
2020
Source
Scientific Reports   10: 3139 (Journal)
Registered Authors
Bitter, Wilbert
Keywords
none
MeSH Terms
  • A549 Cells
  • Animals
  • Bacterial Proteins/metabolism
  • Cluster Analysis
  • Cytoplasm/metabolism*
  • DNA-Directed RNA Polymerases/metabolism
  • Epithelial Cells/microbiology*
  • Gene Expression Regulation, Bacterial
  • Humans
  • Lung/metabolism
  • Models, Genetic
  • Mutation
  • Phosphates/metabolism*
  • Phylogeny
  • Pseudomonas aeruginosa/metabolism*
  • Pulmonary Alveoli/cytology
  • Sigma Factor/metabolism*
  • Signal Transduction
  • Transcriptome
  • Virulence*
  • Virulence Factors/metabolism
  • Zebrafish
PubMed
32081993 Full text @ Sci. Rep.
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.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping