Journal of Bacteriology, November 2004, p. 7460-7465, Vol. 186, No. 21
0021-9193/04/$08.00+0 DOI: 10.1128/JB.186.21.7460-7465.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
School of Molecular and Microbial Biosciences, University of Sydney,1 School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, New South Wales, Australia2
Received 24 March 2004/ Accepted 5 August 2004
The molecular basis of the loss of tryptophan utilization (indole-negative phenotype) of Shigella strains, in effect clones of Escherichia coli, was investigated. Analysis of the tna operon of 23 Shigella strains representing each of the indole-negative serotypes revealed that insertion sequence-mediated insertion and/or deletions damaged the tna operon, leading to inability to convert tryptophan to indole. These events differ for cluster 1, cluster 3, and the outlier Shigella strains, confirming our previous observation of independent origins of these lineages from within E. coli. Parallel loss of the trait and prevalence of indole-negative strains suggest that the trait is deleterious in Shigella strains and advantages those without it.
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