Quorum sensing control of the CPS virulence determinant in Pantoea stewarti, the disease agent of Stewarts wilt disease in corn
Minogue, T.D.; Wehland, M.; Bernhard, F.; Von Bodman, S.B.ck
Phytopathology 91(6 Suppl): S196
2001
ISSN/ISBN: 0031-949X Accession: 035599478
Pantoea stewartii causes Stewart's wilt on sweet corn as a result of vascular occlusion by the bacterial capsular polysaccharide (CPS). CPS synthesis is controlled at two levels. Primary control derives from EsaR-mediated quorum sensing regulation, which couples CPS synthesis to cell growth. Secondary regulation requires transcriptional activation by the RcsA/B transcription complex. Our genetic results indicate that EsaR functions as a repressor, and that strains mutated in the esaR gene are capable of synthesizing large amounts of CPS independently of cell density and acyl-homoserine lactone co-inducer. Interestingly, mutant strains expressing CPS in a deregulated manner are significantly less virulent than the wild type strain. Here, we present biochemical data that support a function for EsaR as a repressor of quorum sensing. We employed electrophoretic mobility shift assays and Biacore surface plasmon resonance to evaluate the DNA binding properties of EsaR for a 20-mer lux box like element in the esaR promoter. In addition, circular dichroism and fluorescence spectroscopy established that AHL binding promotes structural changes in EsaR. These studies support our genetic data. We will discuss a model for EsaR function as a repressor in contrast to related proteins that are signal dependent transcriptional activators.