Abstract
Fis is a versatile DNA binding protein in bacteria. It has been demonstrated in multiple bacteria that Fis plays crucial roles in regulating bacterial virulence factors and optimizing bacterial adaptation to various environments. However, the role of Fis in Pseudomonas aeruginosa virulence as well as gene regulation remains largely unknown. Here, we found that Fis was required for the virulence of P. aeruginosa in a murine acute pneumonia model. Transcriptome analysis revealed that expression of T3SS genes, including master regulator ExsA, was defective in a fis::Tn mutant. We further demonstrate that the continuous transcription of exsC, exsE, exsB, and exsA driven by the exsC promoter was required for the activation of T3SS. Fis was found to specifically bind to the exsB-exsA intergenic region and plays an essential role in the transcription elongation from exsB to exsA. Therefore, we found a novel role of Fis in the regulation of exsA expression.
Highlights
Pseudomonas aeruginosa is a wide-spread Gram-negative opportunistic human pathogen that causes hospital-acquired infections especially in patients with burns, surgical wounds, cancer or cystic fibrosis (Williams et al, 2010; Gellatly and Hancock, 2013)
To examine the role of Fis in the virulence of P. aeruginosa, we infected mice with wild type PA14 or a fis::Tn mutant from the nonredundant library of PA14 transposon mutants (Liberati et al, 2006) in an acute pneumonia model. 14 h post infection, lungs were isolated and the bacterial numbers were determined by serial dilution and plating
Compared to wild type PA14, the mRNA level of Fis was lower in the fis::Tn mutant, but higher in the complemented strain in bacteria at early, mid-log and stationary growth phases (Figure 1C)
Summary
Pseudomonas aeruginosa is a wide-spread Gram-negative opportunistic human pathogen that causes hospital-acquired infections especially in patients with burns, surgical wounds, cancer or cystic fibrosis (Williams et al, 2010; Gellatly and Hancock, 2013). P. aeruginosa causes acute and chronic infections by orchestrating the expression of a variety of virulence factors (Turner et al, 2014; Huber et al, 2016), such as type III secretion system (T3SS) (Anantharajah et al, 2016), iron acquisition (Reinhart and Oglesby-Sherrouse, 2016), biofilm formation (Rybtke et al, 2015) etc., and quorum sensing system (QS) dependent virulence factors such as pyocyanin, rhamnolipids, etc., (Goo et al, 2015; Moradali et al, 2017). Expression of the T3SS genes is directly regulated by ExsA, the activity of which is regulated by a partner-switching mechanism (Diaz et al, 2011).
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