SUMMARY: Chromosomal genes conferring resistance to trimethoprim were transferred from three independently isolated clinical strains of to 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 K12. Mapping studies revealed that one of the resistance determinants was located at a similar position on the chromosome (1 min) to the -type mutations previously described in 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 gene. The mechanisms of trimethoprim resistance in the three clinical isolates studied were more complex and diverse than was expected from previous studies of K12 mutants.


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