Abstract
Pseudomonas aeruginosa is a Gram-negative bacterium that is responsible for a wide range of infections in humans. Colonies employ quorum sensing (QS) to coordinate gene expression, including for virulence factors, swarming motility and complex social traits. The QS signalling system of P. aeruginosa is known to involve multiple control components, notably the las, rhl and pqs systems. In this paper, we examine the las system and, in particular, the repressive interaction of rsaL, an embedded small regulative protein, employing recent biochemical information to aid model construction. Using analytic methods, we show how this feature can give rise to excitable pulse generation in this subsystem with important downstream consequences for rhamnolipid production. We adopt a symmetric competitive inhibition to capture the binding in the lasI–rsaL intergenic region and show our results are not dependent on the exact choice of this functional form. Furthermore, we examine the coupling of lasR to the rhl system, the impact of the predicted capacity for pulse generation and the biophysical consequences of this behaviour. We hypothesize that the interaction between the las and rhl systems may provide a quorum memory to enable cells to trigger rhamnolipid production only when they are at the edge of an established aggregation.
Highlights
Pseudomonas aeruginosa is a common Gram-negative bacterium responsible for a wide range of infections, including those of the urinary and gastrointestinal tract, the skin, and, most prominently, the respiratory system in immunocompromised hosts and sufferers of cystic fibrosis (CF)
P. aeruginosa is a well-studied opportunistic pathogen in many contexts; it is well known for its ability to form biofilms (O’Loughlin et al 2013; Singh et al 2015), its swarming behaviour (Daniels et al 2004; Shrout et al 2006), its rapid acquisition of resistance to antibiotics (Shih and Huang 2002) and its quorum sensing (QS) behaviour (Fuqua et al 2001)
QS in P. aeruginosa is of particular interest because the mechanism is more complex than the originally discovered, prototypical Lux homolog positive-feedback loop (e.g. James et al 2000; Shadel and Baldwin 1991) and the number of genes regulated by QS is large (Sitnikov et al 1995), especially those associated with virulence (O’Loughlin et al 2013)
Summary
Pseudomonas aeruginosa is a common Gram-negative bacterium responsible for a wide range of infections, including those of the urinary and gastrointestinal tract, the skin, and, most prominently, the respiratory system in immunocompromised hosts and sufferers of cystic fibrosis (CF). QS in P. aeruginosa is of particular interest because the mechanism is more complex than the originally discovered, prototypical Lux homolog positive-feedback loop (e.g. James et al 2000; Shadel and Baldwin 1991) and the number of genes regulated by QS is large (Sitnikov et al 1995), especially those associated with virulence (O’Loughlin et al 2013). Mathematical models of QS in Pseudomonas aeruginosa have received a lot of attention. They provide the formalism to summarize current understanding as well as the means to explore mechanisms and evaluate emergent solution behaviour. We develop a model description, employing recent genomic information and bioinformatic techniques, and explore mechanisms for the generation of pulses and memory effects for downstream rhamnolipid production
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