Competitive and cooperative effects in quorum-sensing-regulated galactoglucan biosynthesis in Sinorhizobium meliloti

The symbiotic nitrogen-fixing bacterium Sinorhizobium meliloti possesses the Sin quorum-sensing system based on N-acyl homoserine lactones (AHLs) as signal molecules. The Sin system consists of SinI, the AHL synthase, and SinR, the LuxR-type regulator. This system regulates the expression of a multitude of S. meliloti genes through ExpR, another LuxR-type regulator. Analysis of the activity of the sinI promoter showed that the expression of sinI is dependent on sinR and enhanced by a combination of expR and Sin AHLs. The characterization of the ExpR binding site upstream of sinI and the identification of binding sites upstream of the galactoglucan biosynthesis genes wgaA (expA1) and wgeA (expE1) allowed the definition of a consensus sequence for these binding sites. Based on this consensus, two additional ExpR binding sites in the promoter regions of exoI and exsH, two genes related to the production of succinoglycan, were found. The specific binding of ExpR to the wgaA and wgeA promoters was enhanced in the presence of oxo-C(14)-HL. Positive regulation of the galactoglucan biosynthesis genes by ExpR was shown to be dependent on WggR (ExpG) and influenced by MucR, both of which are previously characterized regulators of these genes. Based on these results, a reworked model of the Sin-ExpR quorum-sensing regulation scheme of galactoglucan production in S. meliloti is suggested.     

Detection of acyl-homoserine lactones by Escherichia and Salmonella

Escherichia and Salmonella do not synthesize quorum-sensing signaling molecules of the N-acyl-l-homoserine lactone (AHL) type but they can detect AHLs produced by other species of bacteria. AHLs are present in the bovine rumen but not in the remainder of the gastrointestinal tract. Enterohemorrhagic E. coli (EHEC) responds to AHLs extracted from the bovine rumen. Salmonella fails to detect AHLs in the gastrointestinal tracts of pathogen-free mice or pigs, suggesting that AHLs are not present. However, Salmonella does detect the AHL production of Yersinia enterocolitica in mouse Peyer's patches. In response to AHLs, EHEC represses flagellar genes and the LEE pathogenicity island while it activates the acid fitness island, whereas Salmonella activates the rck operon and a gene, srgE, encoding a putative Type III secreted effector.