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. Author manuscript; available in PMC: 2009 Feb 9.
Published in final edited form as: Gastroenterology. 2008 Oct 9;136(1):227–235.e3. doi: 10.1053/j.gastro.2008.10.016

Table 3.

λ CII Mutant Analysis

Ung−/− Ung−/−
WT control WT deficient Control deficient
No. of mice 8 10 8 9
Mutants sequenced 108 194 215 213
Sequences with CII mutation 82 158 154 161
Nonredundant eventsa 70 120 133 119
Transition 46 (66%) 63 (53%) 89 (67%) 70 (59%)
C/G → T/A 40 (57%) 49 (41%) 67 (50%) 66 (55%)
non CpG 2 (3%) 8 (7%) 21 (16%) 20 (17%)
at CpG 38 (54%) 41 (34%) 46 (35%) 46 (39%)
T/A → C/G 6 (9%) 14 (12%) 22 (17%) 4 (3%)
Transversion 20 (29%) 43 (36%) 29 (22%) 33 (28%)
C/G → A/T 12 (17%) 24 (20%) 22 (17%) 28 (24%)
C/G → G/C 4 (6%) 6 (5%) 2 (2%) 2 (2%)
T/A → A/T 3 (4%) 8 (7%) 3 (2%) 3 (3%)
T/A → G/C 1 (1%) 5 (4%) 2 (2%) 0
Events at T/A 10 (14%) 27 (23%) 27 (20%) 7 (6%)
Frameshift 4 (6%) 14 (12%) 15 (11%) 16 (13%)
+1 0 1 (1%) 1 (1%) 0
− 1 4 (6%) 13 (11%) 14 (11%) 16 (13%)

WT, wild-type.

a

Identical mutations occurring at the same site in more than one phage from the same mouse (jackpot mutants) were tabulated as a single mutational event. The difference between C:G transition frequency at non–CpG sites of Ung−/− mice and WT mice is significant (P = .0003, Fisher’s exact test). For sequencing and analysis of mutation patterns, all available mutant plaques were used.