Abstract
Three Type VI Secretion System (T6SS) loci called H1- to H3-T6SS coexist in Pseudomonas aeruginosa. H1-T6SS targets prokaryotic cells whereas H2-T6SS mediates interactions with both eukaryotic and prokaryotic host cells. Little is known about the third system, except that it may be connected to H2-T6SS during the host infection. Here we show that H3-T6SS is required for P. aeruginosa PAO1 virulence in the worm model. We demonstrate that the two putative H3-T6SS operons, called “left” and “right”, are coregulated with H2-T6SS by the Las and Rhl Quorum Sensing systems. Interestingly, the RpoN σ54 factor has divergent effects on the three operons. As for many T6SSs, RpoN activates the expression of H3-T6SS left. However, RpoN unexpectedly represses the expression of H3-T6SS right and also H2-T6SS. Sfa2 and Sfa3 are putative enhancer binding proteins encoded on H2-T6SS and H3-T6SS left. In other T6SSs EBPs can act as σ54 activators to promote T6SS transcription. Strikingly, we found that the RpoN effects of H3-T6SS are Sfa-independent while the RpoN mediated repression of H2-T6SS is Sfa2-dependent. This is the first example of RpoN repression of a T6SS being mediated by a T6SS-encoded EBP.
Highlights
Protein secretion is an essential for host colonization by pathogenic bacteria
In Burkholderia thailandensis, the T6SS-5 was shown to be required for virulence in a murine melioidosis model, while inactivation of T6SS-1 rendered B. thailandensis more susceptible to contact with other bacteria [12]
The H1T6SS of the PAO1 strain targets toxins into host bacteria [8,13] and H2-T6SS is involved in interactions with eukaryotic and prokaryotic hosts [14,15]
Summary
Protein secretion is an essential for host colonization by pathogenic bacteria. Multiple systems have evolved in order to secrete proteins into the extracellular medium or directly into target cells [1]. A unique feature of T6SSs is their capacity to deliver toxic proteins into eukaryotic host cells as well as into bacteria [4,5]. These systems were originally thought of as virulence determinants towards eukaryotic host cells [6,7], they have been shown to be unambiguously involved in interbacterial interactions and competition [8]. The anti-prokaryotic T6SSs may facilitate the colonization of specific niches where pathogens can express virulence towards eukaryotic cells. Another striking feature of T6SSs is that multiple distinct T6SS loci are often present in a single genome. In Burkholderia thailandensis, the T6SS-5 was shown to be required for virulence in a murine melioidosis model, while inactivation of T6SS-1 rendered B. thailandensis more susceptible to contact with other bacteria [12]
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