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

Autor: Joaquín R. Otero-Asman, Wilbert Bitter, Kin K. Jim, Cristina Civantos, J. M. Quesada, María A. Llamas, Alain A. Ocampo-Sosa
Přispěvatelé: Ministerio de Economía y Competitividad (España), European Commission, Medical Microbiology and Infection Prevention, AII - Infectious diseases, Graduate School, Molecular Microbiology, AIMMS
Jazyk: angličtina
Rok vydání: 2020
Předmět:
Zdroj: Scientific Reports, Vol 10, Iss 1, Pp 1-13 (2020)
Digital.CSIC. Repositorio Institucional del CSIC
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Scientific Reports, 10(1). Nature Publishing Group
Otero-Asman, J R, Quesada, J M, Jim, K K, Ocampo-Sosa, A, Civantos, C, Bitter, W & Llamas, M A 2020, ' The extracytoplasmic function sigma factor σ VreI is active during infection and contributes to phosphate starvation-induced virulence of Pseudomonas aeruginosa ', Scientific Reports, vol. 10, no. 1, pp. 3139 . https://doi.org/10.1038/s41598-020-60197-x
Scientific reports, 10(1). Nature Publishing Group
Otero-Asman, J R, Quesada, J M, Jim, K K, Ocampo-Sosa, A, Civantos, C & Bitter, W 2020, ' The extracytoplasmic function sigma factor σVreI is active during infection and contributes to phosphate starvation-induced virulence of Pseudomonas aeruginosa ', Scientific Reports, vol. 10, no. 1, pp. 3139 . https://doi.org/10.1038/s41598-020-60197-x
Scientific Reports
ISSN: 2045-2322
DOI: 10.1038/s41598-020-60197-x
Popis: 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.
We thank W. Koudstaal for critical review of the manuscript, A. van der Sar and T. Verboom (AUMC, Amsterdam) for facilitating the work on zebrafish embryos, F. Madrazo (Instituto de Investigación Sanitaria Valdecilla) for assistance with the confocal fluorescence imaging, and R. Tobes (Era7 Bioinformatics) for the RNA-seq bioinformatics analysis. This work was funded by FEDER and the Spanish Ministry of Economy with grants SAF2015-68873-P and BIO2017-83763-P. JOA was supported by the Spanish Ministry of Economy through a FPI fellowship (BES-2013-066301).
Databáze: OpenAIRE
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