Fig. 3.

Capsular rupture and LE-LE and LE-LF cell defects in Crim1^glcr11 mutants. (A,B) Absence of cataract in 2-month-old wild-type mouse lens (A), and dense cataract in age-matched Crim1^glcr11 mutant mouse lens (B). (C,D) Histology of wild-type lens at 2 months shows no ocular abnormality (C), whereas there is severe cataract with posterior lens rupture in the Crim1^glcr11 mutant (D). (E,F) Higher magnification of LE cells shows a thickened anterior capsule (Cap.) and vacuolization and detachment of LE cells from LF cells in Crim1^glcr11 mutants (F), as compared with wild type (E). (G-H′) The morphological phenotype appears as early as P6 as the mutant develops a smaller lens with vacuolization at LE-LF cell junctions (H′), as compared with wild type (G′). (I,J) Quantification of lens width versus length ratio (I) and LE cell number (J) reveals altered morphology and decreased LE cell number in the mutant lens. n=5; ***P<0.001 (Student's t-test). Images shown are representative of four independent experiments.