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. 2007 Oct 8;51(12):4438–4446. doi: 10.1128/AAC.00328-07

TABLE 3.

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

Strain and stock Sourcea Identified mutationb
Antibiotic MIC (μg/ml) of:
Doubling time (min)c Auxotrophyd ne
fusA (EF-G) rplF (L6) KAN STR FA
IN476-IN494 None None 2 6 0.047 24
FusA-SCV
    AH421 IN488 Pro404Arg None 8 12 3 36
    AH288 IN476 Gly617Asp None 16 32 6 53 Hemin 2
    AH294 IN490 Gly628Val None 16 8 2 40
    AH287 IN476 Ala655Glu None 16 48 12 64 Hemin
    AH291 IN484 Arg659His None 24 24 4 43
    AH297 IN492 Ser660Pro None 24 2 53 Hemin
    AH296 IN490 Gly664Ala None 16 8 3 39
    AH292 IN484 Gly666Val None 32 16 6 36
    AH298 IN494 Gly666Val None 32 6 6 37
FusE
    AH422 IN488 None +2 FS at nt 222 128 32 12 81 Menadione
    AH290 IN478 None Duplicate nt 202-293 256 64 8 200 Menadione
    AH420 IN484 None Δ of nt 72-80 256 256 12 150 Menadione
    AH417 IN480 None −1 FS at nt 422 256 256 24 180 Menadione
    AH416 IN476 None Δ of nt 395-398 256 256 48 170 Menadione
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.