Abstract
The bacteria Serratia proteamaculans 94 have a LuxI/LuxR type QS system consisting of AHL synthase SprI and the regulatory receptor SprR. We have previously shown that inactivation of the AHL synthase sprI gene resulted in an increase in the invasive activity of S. proteamaculans correlated with an increased bacterial adhesion. In the present work, the effects of inactivation of the S. proteamaculans receptor SprR are studied. Our results show that inactivation of the receptor sprR gene leads to an increase in bacterial invasion without any increase in their adhesion. On the other hand, inactivation of the sprR gene increases the activity of the extracellular protease serralysin. Inactivation of the QS system does not affect the activity of the pore-forming toxin ShlA and prevents the ShlA activation under conditions of a limited concentration of iron ions typical of the human body. While the wild type strain shows increased invasion in the iron-depleted medium, deletion of its QS system leads to a decrease in host cell invasion, which is nevertheless similar to the level of the wild type S. proteamaculans grown in the iron-rich medium. Thus, inactivation of either of the two component of the S. proteamaculans LuxI/LuxR-type QS system leads to an increase in the invasive activity of these bacteria through different mechanisms and prevents invasion under the iron-limited conditions.
Highlights
Invasion of host cells by the facultative pathogen Serratia proteamaculans 94 arises at the stationary growth phase when the density of the bacterial population is maximal [1].In response to changes in the density of the population, the Quorum Sensing System (QS)regulates gene expression involved in controlling the lifestyle and activity of bacteria, including the activity of their virulence factors
In contrast to the inactivation of the acyl-L-homoserine lactones (AHL) synthase sprI gene [6], inactivation of the regulatory receptor protein sprR gene does not lead to an increase in the expression of the surface protein OmpX, which is responsible for adhesion, and does not affect the activity of protease protealysin, the substrate of which is OmpX
We have shown that inactivation of the AHL synthase sprI gene resulted in a more than fourfold increase in the invasive activity of S. proteamaculans, preceded by the increase in bacterial adhesion to the cell surface [6]
Summary
Invasion of host cells by the facultative pathogen Serratia proteamaculans 94 arises at the stationary growth phase when the density of the bacterial population is maximal [1].In response to changes in the density of the population, the Quorum Sensing System (QS)regulates gene expression involved in controlling the lifestyle and activity of bacteria, including the activity of their virulence factors. Invasion of host cells by the facultative pathogen Serratia proteamaculans 94 arises at the stationary growth phase when the density of the bacterial population is maximal [1]. S. proteamaculans 94 has a LuxI/LuxR type. In a classical Aliivibrio fischeri [2] LuxI/LuxR QS model, AHLs’ binding stabilize the LuxRtype proteins, allowing them to bind DNA and activate transcription of target genes [3], including the LuxI-type AHL synthase gene. In this QS model, expression of the AHL synthase gene requires AHL activation of the LuxR protein.
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