Because of the lack of naturally occurring mutations in exons 1a, 2, 7, 8, 9, 26, 37, 38, and 50, we generated mutagenized amplicons (6) for each of these DNA regions by introducing a conservative transversion
(C [left and right arrow] G or A [left and right arrow] T) in the portion of the fragment displaying the higher melting profile.
The variable sites were comprised of 18 transitions and one transversion
. No heterozygous individuals were found.
Seven polymorphic sites were observed including six transitions and one transversion
. The samples were 13 Arabian, 14 Saudi, 4 English, 1 German, 4 Indian and 10 Hybrids.
anthracis genome (7), coupled with analysis of more than 230 close and diverse isolates, suggests that the pagA 981 transversion
represents a new canSNP that can rapidly identify the closest relatives of this distinct Sverdlovsk lineage.
Nucleotide positions featuring only transitions were most common, followed by positions exhibiting both transitions and transversions
. Positions presenting only transversions
were the least common.
* G/T transversion
in exon 5 at position +5665 (codon 198; Lys198Asn) (5, 7, 8, 12)
When [Kappa] [greater than] 0, transitions are more frequent than transversions
. The diagonals of the rate matrix [q.sub.ii] are specified by the requirement that the row sums of Q are zero.
To identify the mutation saturation in phylogeny, an analysis was conducted using GTR-based models by ploting transitions and transversions
This analysis was carried out with 8:1 weighting, so that eight steps can represent eight transitions or one transversion
Comparison of genotypic statistics using the E1 gene and the molecular epidemiology window (MEW) Intergenotypic distance (a,b) G+C Transition/ Mean Window content (a) transversion
(a) Range Mean RGI vs RGII E1 66.6 6.34 0.08~10.32 4.92 7.28 MEW 66.1 6.15 0~11.69 4.97 8.32 Intragenotypic distances (a,c) RGI RGII Window Range Mean Range Mean E1 0.08~5.75 3.55 0~7.95 5.66 MEW 0~5.97 3.49 0~8.71 6.61 (a) Statistics were determined from all sequences listed in Table 1.
An important hurdle in diagnosis of HC and detection of asymptomatic patients was cleared in 1996, when the gene for HC (HFE gene) was cloned and two causative mutations were reported: the 845G [right arrow] A transition, which changes amino acid 282 from cysteine to tyrosine (C282Y); and the 187C [right arrow] G transversion
, which changes amino acid 63 from histidine to aspartic acid (H63D) (5).
Both transition and transversion
mutations were observed however transversions
were of relatively higher frequency.