Genetic analysis of chromosomal resistance to trimethoprim derived from clinical isolates of Escherichia coli.
Chromosomal genes conferring resistance to trimethoprim were transferred from three independently isolated thy+ clinical strains of Escherichia coli to Escherichia coli K12 by using P1 transduction. Trimethoprim-resistant transductants were obtained less frequently than transductants of other chromosomal markers, suggesting that there were problems related to the expression of the trimethoprim resistance genes in E. coli K12. Mapping studies revealed that one of the resistance determinants was located at a similar position on the chromosome (1 min) to the fol-type mutations previously described in E. coli K12. The two remaining resistance determinants mapped at separate positions between 2.5 and 3 min on the chromosome. The presence of one of these determinants reduced the efficiency with which either donor or recipient cells carrying it could participate in conjugation mediated by the sex factor F and also resulted in phenotypic interaction with the azi gene. The mechanisms of trimethoprim resistance in the three clinical E. coli isolates studied were more complex and diverse than was expected from previous studies of E. coli K12 mutants.
D002874:Chromosome Mapping; D002876:Chromosomes, Bacterial; D003227:Conjugation, Genetic; D004352:Drug Resistance, Microbial; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics* / Q000648:ultrastructure; D005798:Genes, Bacterial; D014161:Transduction, Genetic; D014295:Trimethoprim / Q000494:pharmacology*
D014295:Trimethoprim