A Novel Extracytoplasmic Function (ECF) Sigma Factor Regulates Virulence in Pseudomonas aeruginosa

Next to the two-component and quorum sensing systems, cell-surface signaling (CSS) has been recently identified as an important regulatory system in Pseudomonas aeruginosa. CSS systems sense signals from outside the cell and transmit them into the cytoplasm. They generally consist of a TonB-dependent outer membrane receptor, a sigma factor regulator (or anti-sigma factor) in the cytoplasmic membrane, and an extracytoplasmic function (ECF) sigma factor. Upon perception of the extracellular signal by the receptor the ECF sigma factor is activated and promotes the transcription of a specific set of gene(s). Although most P. aeruginosa CSS systems are involved in the regulation of iron uptake, we have identified a novel system involved in the regulation of virulence. This CSS system, which has been designated PUMA3, has a number of unusual characteristics. The most obvious difference is the receptor component which is considerably smaller than that of other CSS outer membrane receptors and lacks a β-barrel domain. Homology modeling of PA0674 shows that this receptor is predicted to be a bilobal protein, with an N-terminal domain that resembles the N-terminal periplasmic signaling domain of CSS receptors, and a C-terminal domain that resembles the periplasmic C-terminal domains of the TolA/TonB proteins. Furthermore, the sigma factor regulator both inhibits the function of the ECF sigma factor and is required for its activity. By microarray analysis we show that PUMA3 regulates the expression of a number of genes encoding potential virulence factors, including a two-partner secretion (TPS) system. Using zebrafish (Danio rerio) embryos as a host we have demonstrated that the P. aeruginosa PUMA3-induced strain is more virulent than the wild-type. PUMA3 represents the first CSS system dedicated to the transcriptional activation of virulence functions in a human pathogen

The Legume–Rhizobia Symbiosis

The symbiotic nitrogen fixation (SNF) with legumes is the primary source of biologically fixed nitrogen for agricultural system. It is performed by a group of bacteria commonly called rhizobia. It is characterized by a host preference, and the differences among symbioses between rhizobial strains and legume genotypes are related to infection, nodule development and effectiveness in N2 fixation. The interaction between a rhizobia and the legume is mediated by a lipochitin oligosaccharide secreted by the rhizobia, and called “Nod factor”. It is recognized by transmembrane receptors on the root-hair cells of the legume. It can regulate the nodule organogenesis by inducing changes in the cytokinin balance of the root, during nodule initiation. N2 fixation in legume nodules is catalyzed by the nitrogenase enzyme depending upon the photosynthate supply, the O2 concentration, and the fixed-N export. Among environmental factors that influence the SNF, the temperature is essential for nodule formation; the salinity and drought decrease the nodule permeability to O2 and the photosynthate supply to the nodule, the phosphorus deficiency inhibits the nodule development and the total N2 fixation. Rhizobia strains differ in their efficiency in N2 fixation with host legume. There is evidence of genotypic variability for SNF at different levels of available P which show a possibility of selecting cultivars able to support biological N2 fixation under low P soils