PpoR, an orphan LuxR-family protein of Pseudomonas putida KT2440, modulates competitive fitness and surface motility independently of N-acylhomoserine lactones

Pseudomonas putida KT2440 does not produce any of the common molecules involved in quorum sensing signalling described in other bacteria. However, as is the case in other microorganisms, the genome of this strain contains an open reading frame (PP_4647) coding for a transcriptional regulator belonging to the LuxR protein family. In this article, we present evidence indicating that this protein, named PpoR, modulates swarming motility in KT2440 and plays a role in the survival of this strain in the presence of potential competitors. These functions appear to be independent of known N-acylhomoserine lactones (AHLs), since we show that P. putida KT2440 does not produce significant quantities of these molecules under any condition tested and PpoR does not influence the expression of quorum sensing-dependent promoters even in the presence of exogenous AHLs. A ppoR mutant shows increased sensitivity to the iron chelator 2,2'-dipyridyl, while iron supplementation compensates the fitness loss of the mutant in competition with other Pseudomonas. All these data suggest that PpoR participates in both inter- and intraspecific processes relevant to the fitness of P. putida related to iron acquisition, and not necessarily mediated by canonical quorum sensing signal molecules.