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Title: A CELL SURFACE POLYSACCHARIDE THAT FACILITATES RAPID POPULATION MIGRATION BY DIFFERENTIATED SWARM CELLS OF PROTEUS MIRABILIS

Author
item GYGI, DANIEL - UNIVERSITY OF CAMBRIDGE
item RAHMAN, M. - UNIVERSITY OF GEORGIA
item LAI, HSIN-CHIH - UNIVERSITY OF CAMBRIDGE
item CARLSON, RUSSELL - UNIVERSITY OF GEORGIA
item PETTER, JEAN
item HUGHES, COLIN - UNIVERSITY OF CAMBRIDGE

Submitted to: Journal of Molecular Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/26/1995
Publication Date: N/A
Citation: N/A

Interpretive Summary: Swarming migration by gram-negative organisms, including some food-borne pathogens, is a process where bacteria produce tremendous numbers of complex molecules that enable them to travel long distances across dry surfaces to new sources of nutrients. When bacteria enter a swarming phase, in addition to producing molecules associated with migration, many new virulence-associated proteins are expressed in a coordinated fashion that include hemolytic toxins and antibody-degrading proteases. Though not a food-borne pathogen, Proteus mirabilis is the model organism for understanding how swarming increases invasion and virulence. For this reason, mutations were made in P. mirabilis genes that only stopped migration but did not effect the expression of the virulence-associated proteins. The results showed that production of a carbohydrate capsule was crucially involved in migration, and its presence was a primary reason n that the bacteria could be virulent. These results emphasize the importance of complex carbohydrates in making bacteria capable of causing disease.

Technical Abstract: Swarming by Proteus mirabilis is characterised by cycles of rapid population migration across surfaces, following differentiation of typical vegetative rods into long, hyperflagellated, virulent swarm cells. A swarm-defective TnphoA insertion mutant was isolated that was not defective in cell motility, differentiation or control of the migration cycle, but was specifically impaired in the ability to undergo surface translocation as a multicellular mass. The mutation, previously shown to compromise urinary tract virulence, was located within a 1112bp gene that restored normal swarming of the mutant when expressed in trans. The gene encoded a 40.6kDa protein that is related to putative sugar transferases required for lipopolysaccharide (LPS) core modification in Shigella and Salmonella. The immediately distal open reading frame encoded a protein that is related to dehydrogenases involved in the synthesis of LPS O-side chains, enterobacterial common antigen and extracellular polysaccharide (PS). Gel electrophoresis and electron microscopy showed that the mutant still made LPS but it had lost the ability to assemble a surface (capsular) PS, which gas liquid chromatography and mass spectrometry indicated to be an acidic type II molecule rich in galacturonic acid and galactosamine. We suggest that this surface PS facilites translocation of differentiated cell populations by reducing surface friction.