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. 1994 Oct;176(20):6229–6237. doi: 10.1128/jb.176.20.6229-6237.1994

Mechanism of bacitracin resistance in gram-negative bacteria that synthesize exopolysaccharides.

T J Pollock 1, L Thorne 1, M Yamazaki 1, M J Mikolajczak 1, R W Armentrout 1
PMCID: PMC196963  PMID: 7928993

Abstract

Four representative species from three genera of gram-negative bacteria that secrete exopolysaccharides acquired resistance to the antibiotic bacitracin by stopping synthesis of the exopolysaccharide. Xanthomonas campestris, Sphingomonas strains S-88 and NW11, and Escherichia coli K-12 secrete xanthan gum, sphingans S-88 and NW11, and colanic acid, respectively. The gumD gene in X. campestris is required to attach glucose-P to C55-isoprenyl phosphate, the first step in the assembly of xanthan. A recombinant plasmid carrying the gumD gene of X. campestris restored polysaccharide synthesis to bacitracin-resistant exopolysaccharide-negative mutants of X. campestris and Sphingomonas strains. Similarly, a newly cloned gene (spsB) from strain S-88 restored xanthan synthesis to the same X. campestris mutants. However, the intergeneric complementation did not extend to mutants of E. coli that were both resistant to bacitracin and nonproducers of colanic acid. The genetic results also suggest mechanisms for assembling the sphingans which have commercial potential as gelling and viscosifying agents.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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