Quorum Sensing Regulates Exopolysaccharide Production, Motility, and Virulence in Pseudomonas syringae

Abstract

The N-acyl homoserine lactone (AHL)-mediated quorum-sensing system in the phytopathogen Pseudomonas syringae pv. syringae requires the AHL synthase AhlI and the regulator AhlR, and is additionally subject to regulation by AefR. The contribution of quorum sensing to the expression of a variety of traits expected to be involved in epiphytic fitness and virulence of P syringae were examined. Both an aefR- mutant and an ahlI- ahlR- double mutant, deficient in AHL production, were significantly impaired in alginate production and had an increased susceptibility to hydrogen peroxide compared with the wild-type strain. These mutants were hypermotile in culture, invaded leaves more rapidly, and caused an increased incidence of brown spot lesions on bean leaves after a 48-h moist incubation. Interestingly, an aefR- mutant was both the most motile and virulent. Like the wild-type strain, the AHL-deficient mutant strains incited water-soaked lesions on bean pods. However, lesions caused by an ahlI- ahlR- double mutant were larger, whereas those incited by an aefR- mutant were smaller. In contrast, tissue maceration of pods, which occurs at a later stage of infection, was completely abolished in the AHL-deficient mutants. Both the incidence of disease and in planta growth of P syringae pv. tabaci were greatly reduced in transgenic tobacco plants that produced AHL compared with wild-type plants. These results demonstrate that quorum sensing in E syringae regulates traits that contribute to epiphytic fitness as well as to distinct stages of disease development during plant infection.

A Homologue of the 3-Oxoacyl-(Acyl Carrier Protein) Synthase III Gene Located in the Glycosylation Island of Pseudomonas syringae pv. tabaci Regulates Virulence Factors via N -Acyl Homoserine Lactone and Fatty Acid Synthesis

“…The ⌬psyI mutant showed the same level of swarming ability as the WT, although AHL-deficient mutants of P. syringae pv. syringae B728a exhibited high motility (25). Because this mutant is defective in both the ahlI and ahlR genes, which encode an AHL synthetic enzyme and a transactivator of AHL-responsive genes, the phenotype might be different from that caused by our single mutation of psyI in P. syringae pv.…”

“…EPS production and tolerance to H 2 O 2 and antibiotics. Previous papers have reported that the production of EPS is regulated by quorum sensing and that an EPS-deficient mutant of P. syringae is hypersensitive to environmental stresses (7,17,25). To compare extracellular polysaccharide production on an MMMF plate with 1.5% agar after 48 h of incubation at 27°C, each mutant was scraped off and the amounts of extracellular polysaccharide and extracellular proteins as an internal control were quantified (Fig.…”

“…It was reported that a P. syringae mutant defective in EPS production was hypersensitive to H 2 O 2 (17,25). In P. syringae pv.…”

Defects in flagellin glycosylation affect the virulence of Pseudomonas syringae pv. tabaci 6605

“…It was reported that a mutant of P. syringae deficient in EPS production had enhanced sensitivity to H 2 O 2 (Keith & Bender, 1999;Daniels et al, 2004;Quinones et al, 2005), and the Dorf3 mutant of P. syringae pv. tabaci 6605 had enhanced tolerance to H 2 O 2 and antibiotics due to the overexpression of EPS (Taguchi et al, 2006a).…”

The effect of pmpR on the type III secretion system in Pseudomonas aeruginosa

“…aeruginosa possesses at least 2 well-defined acylhomoserine lactone (HSL)-based quorum-sensing systems, las and rhl, which control numerous virulence factor genes including lasA, lasB, and rhlA [1,2]. Each system comprises a transcriptional activator and an autoinducer synthase.…”