TABLE 3.

Mutants selected as Kanr SCVs in FA-susceptible clinical isolates and then screened for FA resistance

Strain and stockSourceaIdentified mutationbAntibiotic MIC (μg/ml) of:Doubling time (min)cAuxotrophydne
fusA (EF-G)rplF (L6)KANSTRFA
IN476-IN494NoneNone260.04724
FusA-SCV
    AH421IN488Pro404ArgNone812336
    AH288IN476Gly617AspNone1632653Hemin2
    AH294IN490Gly628ValNone168240
    AH287IN476Ala655GluNone16481264Hemin
    AH291IN484Arg659HisNone2424443
    AH297IN492Ser660ProNone24253Hemin
    AH296IN490Gly664AlaNone168339
    AH292IN484Gly666ValNone3216636
    AH298IN494Gly666ValNone326637
FusE
    AH422IN488None+2 FS at nt 222128321281Menadione
    AH290IN478NoneDuplicate nt 202-293256648200Menadione
    AH420IN484NoneΔ of nt 72-8025625612150Menadione
    AH417IN480None−1 FS at nt 42225625624180Menadione
    AH416IN476NoneΔ of nt 395-39825625648170Menadione
  • a Each of the original FA-susceptible clinical isolates had similar MICs for KAN, STR, and FA and similar doubling times in LB.

  • b None, wild type. FS, frameshift mutation.

  • c Doubling time (generation time) in minutes during exponential growth in LB.

  • d Auxotrophy tested for hemin, menadione, thymine, and thymidine. −, nonauxotrophic.

  • e Number of independent isolates with same genotype and phenotype.