Abstract
In many Gram-negative bacteria, virulence, and social behavior are controlled by quorum-sensing (QS) systems based on the synthesis and perception of N-acyl homoserine lactones (AHLs). Quorum-quenching (QQ) is currently used to disrupt bacterial communication, as a biocontrol strategy for plant crop protection. In this context, the Gram-positive bacterium Rhodococcus erythropolis uses a catabolic pathway to control the virulence of soft-rot pathogens by degrading their AHL signals. This QS signal degradation pathway requires the expression of the qsd operon, encoding the key enzyme QsdA, an intracellular lactonase that can hydrolyze a wide range of substrates. QsdR, a TetR-like family regulator, represses the expression of the qsd operon. During AHL degradation, this repression is released by the binding of the γ-butyrolactone ring of the pathogen signaling molecules to QsdR. We show here that a lactone designed to mimic quorum signals, γ-caprolactone, can act as an effector ligand of QsdR, triggering the synthesis of qsd operon-encoded enzymes. Interaction between γ-caprolactone and QsdR was demonstrated indirectly, by quantitative RT-PCR, molecular docking and transcriptional fusion approaches, and directly, in an electrophoretic mobility shift assay. This broad-affinity regulatory system demonstrates that preventive or curative quenching therapies could be triggered artificially and/or managed in a sustainable way by the addition of γ-caprolactone, a compound better known as cheap food additive. The biostimulation of QQ activity could therefore be used to counteract the lack of consistency observed in some large-scale biocontrol assays.
Highlights
Many human, animal, and plant pathogens use quorum-sensing (QS) systems to coordinate their virulent social behavior and overwhelm host defenses (von Bodman et al, 2003; Papenfort and Bassler, 2016)
We investigated the artificial induction of qsd operon transcription implicated in rhodococcal QQ activity, by adding GCL to the R. erythropolis R138 culture at mid-exponential growth phase, as described for the GCL degradation kinetics assays
Rhodococcus erythropolis is a bacterial species characterized by a remarkable metabolic versatility, with specific enzymes for degrading recalcitrant and xenobiotic compounds (Martínková et al, 2009; Polkade et al, 2016; Ceniceros et al, 2017; Kim et al, 2018; Zampolli et al, 2019)
Summary
Animal, and plant pathogens use quorum-sensing (QS) systems to coordinate their virulent social behavior and overwhelm host defenses (von Bodman et al, 2003; Papenfort and Bassler, 2016). Hraiech et al (2014) used SsoPox lactonase inhalation therapy to inhibit QS in Pseudomonas aeruginosa, thereby decreasing mortality in a rat model of pneumonia. Such quorum-quenching (QQ) approaches aim to decrease the expression of virulence rather than limiting cell growth or eradicating pathogens (Faure and Dessaux, 2007). At first glance, they are highly attractive, as they should exert less selective pressure on bacterial populations than antibiotics. In situations in which it is not relevant or possible to use QS inhibitors or QQ enzyme extracts against virulent bacteria, an alternative approach can be adopted in which the production of QQ enzymes of antagonistic bacteria is boosted directly in their ecological niche (Uroz et al, 2009), as proposed here
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