An SbmA mutation in E. coli Tn10–carrying strains results in hypersusceptibility to tetracycline

RICARDO DE CRISTÓBAL; PAULA VINCENT; RAÚL SALOMÓN

Rosario, Argentina

Congreso; XLII reunión anual de la sociedad argentina de investigaciones en bioquímica y biología molecular; 2006

sociedad argentina de investigaciones en bioquímica y biología molecular

The Escherichia coli sbmA gene product is involved in uptake of microcins B17 and J25, but its physiological role is still unknown. We have found that an E. coli sbmA::Tn5 mutant harboring a Tn10 transposon does not form isolated colonies in the presence of as low a concentration of tetracycline as 5 mg/ml, in spite of the presence of the Tn10 transposon. When a culture of the sbmA mutant was grown in LB, serially diluted, and aliquots of 10-2 and 10-3 dilutions spread on LB-Tc plates there was confluent growth. However, 10-4 and higher dilutions resulted in no single colonies. One explanation for these findings is that as the plates become increasingly crowded the ability of the mutant to divide normally in the presence of tetracycline is restored. An interpretation of this observation is that cells release a factor that diffuses to other cells and stimulates their growth and division. Thus, a certain number of neighboring cells would be required in order to reach a high local concentration of the factor. Below a critical number of cells they should fail to develop into a colony because they are unable to signal to themselves. What is not yet clear is the mechanism by which the mutation abolish the resistance conferred by the transposon and how it is restored by the putative factor. Our results could throw light on the natural role of SbmA.