The focus of our research is to study signaling mechanisms that lead to differentiation of S.typhimurium into hyperfiagellated swarmer cells when propagated on a solid growth surface. Knowledge gained from these studies will be extended to the area of bioflims and virulence. A swarmer colony secretes 'slime' which is mainly composed of polysaccharides; biofilms are bacterial colonies within 'slime layers', which play an important role in the persistence of infections. Our current hypothesis is that slime is essential for swarming in at least two ways: provides the milieu for swarming motility, and constitutes the signal for swarmer cell differentiation. Preliminary results have ruled out signals such as specific amino acids, pH changes, oxygen, iron starvation, increased viscosity, flagellar rotation or known autoinducer systems. Extensive transposon mutagenesis has led to the isolation of swarming mutants, a majority of which were defective in lipopolysaccharide (LPS) synthesis, a large number defective in the chemotaxis signaling pathway, and some defective in putative two-component signaling components. A mutation in waaG (LPS core modification): secreted copious amounts of slime and showed a precocious swarming phenotype. We have suggested that the 0-antigen improves surface 'wettability' required for swarm colony expansion, that the LPS core could play a: role in slime generation, and that multiple two-component systems cooperate to promote swarmer cell differentiation. We propose to 1. Investigate the role of the well-understood chemotaxis signaling system in swarmer cell differentiation, 2. Investigate roles of two of the newly implicated two-component signaling systems in swarming and in virulence, and 3. Test polysaccharides as potential swarming signals, and understand the relationship between slime elaborated by moving swarmer cells and that secreted by adherent bacteria in bioflims.
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