The production of these compounds is associated with hypo-osmotic stress tolerance in rhizobia [47]. The higher sensitivity of the rosR mutants to hypo-osmotic stress might be explained by increased check details permeability of their cell envelopes, which could allow excretion of greater amounts of neutral polysaccharides. Recently, several other osmotically unstable rhizobial mutants have been described, among them salt-sensitive mutants of S. meliloti, some of them significantly affected in competing against the wild type for nodule occupancy [48]. Mutation in S. meliloti regulatory gene nesR affected competition for nodulation, adaptation to high osmolarity, and nutrient

starvation [49]. Also, genes encoding trehalose biosynthesis pathways and potassium uptake systems were found to be important for S. meliloti growth in hyperosmotic medium [50, 51]. R. leguminosarum bv. trifolii rosR mutants deficient in EPS production grew considerably slower than the wild type on minimal medium. Using the Biolog system, we established that the rosR mutant revealed differences in utilization of carbon and nitrogen sources in relation to the wild

type. Similarly, phenotypic analysis of S. meliloti exoS and chvI null mutants demonstrated that ExoS/ChvI regulatory system not only controls succinoglycan (EPS I) and galactoglucan (EPS II) synthesis but is also required for growth on over 21 different carbon sources [52]. Molecular motor The chvI mutant exhibited Batimastat datasheet several pleiotropic effects: failed to grow on complex medium, had an altered LPS profile, exhibited lower tolerance to acidic conditions, was hypermotile, and synthesized significantly less poly-3-hydroxybutyrate than wild type, indicating that ChvI is engaged in regulatory networks involving the cell envelope and metabolism [53]. In several studies, a connection between the production of bacterial polysaccharides and motility has been established. Both R. leguminosarum bv. trifolii

rosR mutants and the pssA mutant deficient in EPS production exhibited a significant decrease in motility. S. meliloti MucR protein that simultaneously acts as a transcriptional repressor of galactoglucan synthesis and an activator of succinoglycan synthesis [25, 54] inhibits the expression of rem encoding an activator of the expression of such genes as flaF and flgG [55]. Other regulatory proteins, such as the ExpR/Sin quorum system, are additionally engaged in the regulation of S. meliloti motility [56, 57]. A non-motile phenotype has also been described for ndvA and ndvB mutants defective in the synthesis of β-(1,2)-glucans under hypo-osmotic conditions [58, 59]. Alterations in the LPS structure often cause motility-related defects [60, 61]. The R. leguminosarum bv. viciae 3841 LPS mutant mentioned earlier was impaired in motility and biofilm formation.