Genesis of a complex transposon encoding the OXA-1 (type II) beta-lactamase gene.
Plasmid R753-1-encoded resistance to ampicillin (by production of OXA-1 [type II] beta-lactamase), streptomycin, and sulfonamide was analyzed functionally and physically. The OXA-1 beta-lactamase gene on R753-1 could not transpose, whereas on some plasmids this gene was capable of transposition as part of transposon Tn2603. By using the nontransposable gene on R753-1 with Tn21 on a separate plasmid, we observed the genesis of a complex transposon with a structure similar to that of Tn2603. This finding confirms our previous hypothesis that Tn2603 has evolved directly from Tn21 through acquisition of the OXA-1 beta-lactamase gene by substitution of DNA segments. Furthermore, the mechanism of mobilization of pACYC184 derivatives by RecA-dependent homologous recombination was demonstrated.
D005075:Biological Evolution; D002874:Chromosome Mapping; D004262:DNA Restriction Enzymes; D004251:DNA Transposable Elements; D004269:DNA, Bacterial / Q000235:genetics; D004352:Drug Resistance, Microbial; D004926:Escherichia coli / Q000235:genetics*; D005798:Genes, Bacterial; D009693:Nucleic Acid Hybridization; D011815:R Factors; D011995:Recombination, Genetic; D001618:beta-Lactamases / Q000235:genetics*
D004251:DNA Transposable Elements; D004269:DNA, Bacterial; D004262:DNA Restriction Enzymes; D001618:beta-Lactamases