The cell density‐dependent expression of stewartan exopolysaccharide in Pantoea stewartii ssp. stewartii is a function of EsaR‐mediated repression of the rcsA gene

• Published in: Molecular microbiology Vol. 56; no. 1; pp. 189 - 203
• Main Authors: Minogue, Timothy D., Carlier, Aurelien L., Koutsoudis, Maria D., Von Bodman, Susanne B.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.04.2005; Blackwell Science; Blackwell Publishing Ltd
• Subjects: 4-Butyrolactone - analogs & derivatives; 4-Butyrolactone - metabolism; Bacterial Proteins - chemistry; Bacterial Proteins - genetics; Bacterial Proteins - metabolism; Bacteriology; Base Sequence; Biological and medical sciences; Crop diseases; Deoxyribonucleic acid; DNA; Escherichia coli Proteins - genetics; Escherichia coli Proteins - metabolism; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation, Bacterial; Genes; Gram-positive bacteria; Microbiology; Miscellaneous; Molecular Sequence Data; Pantoea - genetics; Pantoea - growth & development; Pantoea - metabolism; Pantoea - pathogenicity; Pantoea stewartii; Plant Diseases - microbiology; Polysaccharides, Bacterial - metabolism; Signal Transduction; Transcription Factors - chemistry; Transcription Factors - genetics; Transcription Factors - metabolism; Zea mays - microbiology; Bacteria; Pantoea stewartii; Gene; Microbiology; Enterobacteriaceae
• DOI: 10.1111/j.1365-2958.2004.04529.x
• ISSN: 0950-382X

Summary The LuxR‐type quorum‐sensing transcription factor EsaR functions as a repressor of exopolysaccharide (EPS) synthesis in the phytopathogenic bacterium Pantoea stewartii ssp. stewartii. The cell density‐dependent expression of EPS is critical for Stewart's wilt disease development. Strains deficient in the synthesis of a diffusible acyl‐homoserine lactone inducer remain repressed for EPS synthesis and are consequently avirulent. In contrast, disruption of the esaR gene leads to hypermucoidy and attenuated disease development. Ligand‐free EsaR functions as a negative autoregulator of the esaR gene and responds to exogenous acyl‐homoserine lactone for derepression. The focus of this study was to define the mechanism by which EsaR governs the expression of the cps locus, which encodes functions required for stewartan EPS synthesis and membrane translocation. Genetic and biochemical studies show that EsaR directly represses the transcription of the rcsA gene. RcsA encodes an essential coactivator for RcsA/RcsB‐mediated transcriptional activation of cps genes. In vitro assays identify an EsaR DNA binding site within the rcsA promoter that is reasonably well conserved with the previously described esaR box. We also describe that RcsA positively controls its own expression. Interestingly, promoter proximal genes within the cps cluster are significantly more acyl‐homoserine lactone responsive than genes located towards the middle or 3′ end of the gene cluster. We will discuss a possible role of EsaR‐mediated quorum sensing in the differential expression of the cps operon.