Skip to main content
. 2007 May 18;189(15):5728–5737. doi: 10.1128/JB.00161-07

TABLE 3.

rpoB mutation spectra of N. meningitidis H44/76 wild-type and DNA repair-deficient strainsa

H44/76 strain genotype Nucleotide change(s)
Wild typeb GC → AT(103 × 3)
fpg GC → AT(92 × 3)
mutS GC → AT(103 × 2); GC → CG(104 × 1)
dinB GC → AT(92 × 1, 103 × 1, 119 × 1)
uvrA GC → AT(92 × 1, 103 × 1, 119 × 1)
recA6c GC → AT(92 × 2)
mutS dinB GC → AT(92 × 1, 103 × 1); GC → CG(104 × 1)
mutS recA6 GC → AT(92 × 1, 103 × 1); GC → CG(104 × 1)
mutS uvrA GC → AT(92 × 1, 103 × 2)
fpg uvrA GC → AT(92 × 2); GC → TA(103 × 1)
dinB uvrA GC → AT(103 × 3)
dinB recA6 GC → AT(119 × 1); GC → CG(104 × 1); GC → TA(103 × 1)
recA6 uvrA GC → AT(103 × 3)
mutYb GC → TA(92 × 1, 103 × 1, 119 × 1)
mutY fpg GC → TA(92 × 1, 103 × 2)
mutY mutS GC → TA(103 × 3)
mutY dinB GC → TA(103 × 3)
mutY uvrA GC → TA(92 × 1, 103 × 2)
mutY recA6 GC → TA(64 × 1, 103 × 2)
a

Three independent rifampin-resistant strains of the MC H44/76 wild-type and DNA repair-deficient strains listed in Table 1 were analyzed for nucleotide changes conferring rifampin resistance. Subscripts indicate the nucleotide being changed (where nucleotide 1 corresponds to the first nucleotide in the sequencing primer) and the number of strains (× n) with the given transition/transversion.

b

Previously shown by Davidsen et al. (10).

c

One strain showed no nucleotide changes inside the sequenced area.