Transposition of ampicillin resistance to an enterotoxin plasmid in an Escherichia coli strain of human origin.
We examined a strain of Escherichia coli, serotype O159.H34, of human origin which produced heat-stable and heat-labile enterotoxins, was resistant to ampicillin, and produced colicin. By conjugation and transformation experiments plasmids coding for enterotoxin production (Ent), enterotoxin production and ampicillin resistance (Ap-Ent), ampicillin resistance (Ap), and colicin production were isolated. Both the Ent and Ap-Ent plasmids were autotransferring and belonged to the F-incompatibility complex. However, the Apr Ent+ transconjugants showed differences in their levels of resistance and in their abilities to propagate F-specific phages and to transfer resistance. The results suggested there was transposition from the small Ap plasmid to the Ent plasmid. The Ap-Ent plasmids were larger than the enterotoxin factor and when treated with restriction endonuclease BamHI showed an additional fragment not present in the enterotoxin plasmid. The insertion of ampicillin resistance probably occurred at different sites on the enterotoxin plasmid, resulting in the observed variation in phenotype.
D000667:Ampicillin / Q000494:pharmacology*; D001427:Bacterial Toxins / Q000096:biosynthesis*; D003087:Colicins / Q000096:biosynthesis; D003227:Conjugation, Genetic; D004768:Enterotoxins / Q000096:biosynthesis*; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D010957:Plasmids; D011815:R Factors; D011995:Recombination, Genetic
D001427:Bacterial Toxins; D003087:Colicins; D004768:Enterotoxins; D000667:Ampicillin