Summary: K30 produces a thermostable group I capsular polysaccharide. Two classes of mutants were isolated with defects in the synthesis or expression of capsule. The most common mutant phenotype was acapsular (K), with no K-antigen synthesized. A second class of mutants, termed Ki or intermediate forms, produced colonies which were indistinguishable from those of acapsular forms yet K-antigenicity was expressed. Previous studies had demonstrated that strains that produce K30 antigen synthesize a lipopolysaccharide (LPS) fraction that is recognised by monoclonal antibodies against the K30 antigen. Synthesis of this LPS fraction was not affected in Ki forms. The results of morphological examination, LPS analysis and phage sensitivity studies are consistent with the interpretation that the defect in Ki strains results from an inability to polymerize the K30 antigen. Using plasmid pULB113 (RP4 :: mini-Mu), mutations resulting in both K and Ki phenotypes were localized near the region of the chromosome.


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