Table 3.
Suture Defects in Transgenic Mice Compared with Age-Matched Nontransgenic Control Mice
Grade of Sutural Defect
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Transgenic Line | Genotype | Lenses (n) | Grade 0 | Grade I | Grade II | Grade III |
Line 8168 (R116C) | Tg* | 54 | 12 (22) | 15 (28) | 17 (31) | 10 (19) |
Control | 50 | 29 (58) | 16 (32) | 5 (10) | 0 (0) | |
Line 8165 (R116C) | Tg* | 74 | 12 (16) | 24 (32) | 25 (34) | 13 (18) |
Control | 46 | 35 (76) | 7 (15) | 3 (7) | 1 (2) | |
Line 8170 (R116C) | Tg* | 72 | 25 (34) | 7 (10) | 31 (43) | 9 (13) |
Control | 62 | 41 (66) | 12 (19) | 9 (15) | 0 (0) | |
Line 10694 (wild type) | Tg | 62 | 52 (84) | 6 (10) | 2 (3) | 2 (3) |
Control | 70 | 53 (76) | 11 (16) | 3 (4) | 3 (4) |
Lenses were examined ex vivo by stereomicroscopy under dark-field illumination. Sutural defects were graded according to the maximum width of a gap at the posterior suture. Grades were 0, no gap; I, gap width is < 15 μm; II, gap width is 16 to 30 μm; III, gap width is > 30 μm. Tg, transgenic animals; controls were age-matched nontransgenic littermates. Scores were not significantly different among lenses examined at the ages of 9 to 11 weeks, 20 to 22 weeks, and 28 to 30 weeks. Therefore, data from all age groups were pooled. Data are number of lenses, with percentage of total group in parentheses. For the purpose of statistical analyses, grades II and III are combined. Test results for interaction between level of gene expression and severity of suture defects (transgenic group only) were not significant (P = 0.05).
Distribution of severity of lens defect differed between transgenic and control mice (P < 0.05).