A NEGATIVE REGULATOR MEDIATES QUORUM-SENSING CONTROL OF EXOPOLYSACCHARIDE PRODUCTION IN PANTOEA-STEWARTII SUBSP STEWARTII

Classical quorum sensing (autoinduction) regulation, as exemplified by the lux system of Vibrio fischeri, requires N-acyl homoserine lactone (AHL) signals to stimulate cognate transcriptional activators for the cell density-dependent expression of specific target gene systems, Fo r Pantoea stewartii subsp, stewartii, a bacterial pathogen of sweet co rn and maize, the extracellular polysaccharide (EPS) stewartan is a ma jor virulence factor, and its production is controlled by quorum sensi ng in a population density-dependent manner, Two genes, esaI and esaR, encode essential regulatory proteins for quorum sensing. EsaI is the AHL signal synthase, and EsaR is the cognate gene regulator, esaI, Del ta esaR, and Delta esaI-esaR mutations were constructed to establish t he regulatory role of EsaR, We report here that strains containing an esaR mutation produce high levels of EPS independently of cell density and in the absence of the AHL signal. Our data indicate that quorum-s ensing regulation in P. s. subsp. stewartii, in contrast to most other described systems, uses EsaR to repress EPS synthesis at low cell den sity, and that derepression requires micromolar amounts of AHL, In add ition, derepressed esaR strains, which synthesize EPS constitutively a t low cell densities, were significantly less virulent than the wild t ype parent. This finding suggests that quorum sensing in P. s. subsp. stewartii may be a mechanism to delay the expression of EPS during the early stages of infection so that it does not interfere with other me chanisms of pathogenesis.