The production of Pseudomonas syringae pv. syringae’s AHL signal, 3-oxo-hexanoyl-homoserine lactone (3O-C6-HSL), requires the expression of the AHL synthase gene, ahlI, and the AHL regulator gene, ahlR. This AhlI-AhlR quorum sensing system has been demonstrated to be key in controlling traits that contribute to epiphytic fitness, such as exopolysaccharide production, and motility, as well as contributing to disease development during plant infection. The AhlI-AhlR quorum sensing system also is subject to modulation by additional regulatory proteins. A novel regulator, fqsR, was identified as a positive regulator of AHL production. FqsR mutant had a delay in the lag-phase of its growth. Both a fqsR mutant and an ahlI mutant were significantly increased in pyoverdin production and they were hypermotile compared with the wild-type strain. The tobacco HR reaction in the case of ahlI mutant was faster and stronger than fqsR mtant and wild type. The mutants caused water soaked and necrotic lesions on bean pods like the wild-type strain but lesions caused by ahlI mutant were larger than wild-type wherease those incited by a fqsR mutant were larger than WT and smaller than ahlI mutant. Complementation of the fqsR mutant in trans showed higher production of signal molecules. Interestingly, QRT-PCR showed expression of fqsR mutant is under control of quorum sensing suggesting this gene is part of quorum sensing circuity in P. syringae pv. syringae B728a. The above results suggest that the fqsR gene is important for P. syringae to modulate fitness and quorum sensing.

Keywords