Plasmid-mediated suppression of the mutational activation of the bgl operon in Shigella sonnei.

Abstract

SSOR, a clinical isolate of Shigella sonnei which exhibits a Salicin-negative phenotype, is unable to mutate to give rise to Sal+ derivatives although a homolog of the Escherichia coli bgl operon is retained by the strain. This was correlated to the presence of an endogenous plasmid in the strain. A plasmid-cured derivative, AK711, could give rise to Sal+ mutants in two steps. Introduction of the plasmid DNA, extracted from SSOR, into various strains of E. coli and S. sonnei, resulted in ampicillin resistant transformants. Interestingly, the presence of the plasmid suppressed the mutational activation of the bgl operon in the transformants. This was further substantiated by the observation that, transformants that have lost the plasmid regained the ability for mutational activation of the bgl operon. Preliminary characterisation of the plasmid indicated a size of 3.8 kb with an origin of replication resembling that of ColE1 replicons and the bla gene homolog of Tn3. Observations of the mutation frequency at the srl and lac loci in the presence of the plasmid indicate that there is a reduction in the mutation frequency, suggesting an antimutator activity associated with the plasmid.