Search Criteria: Research Area is "Sensorineural Research: Cataracts (cortical)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 001649 | A.BY H2bc H2-T18f/SnJ-Dstncorn1/J | Repository- Live |
| Mice homozygous for the recessive Dstncorn1 mutation have abnormally proliferative basal corneal epithelial cells. Focal areas of corneal epithelial hyperplasia are found by one week of age, and neovascularization is found by 14 days of age when the eyes open. This neovascularization, which progresses during the first two months of age, is not found in mice homozygous for the Dstncorn-2J allele (which is a point mutation leading to a change in a single amino acid residue). In both mutants the corneal epithelial cells show increased levels and altered organizational pattern of filamentous actin. The areas of thickened cortical epithelia yield a roughened, opaque corneal surface. At 4 weeks of age in Dstncorn1 homozygotes, expression of keratin 14 and involucrin extend into the suprabasal layer in the areas of hyperplastic corneal epithelia. There is also an increase in the levels of expression of cofilin 1, lumican and kerat
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| 000391 | B6EiC3Sn a/A-Pax6Sey-Dey/J | Repository- Live |
| Mice homozygous for the spontaneous semidominant Dickie's small eye mutation(Pax6Sey-Dey) die during embryogenesis. Heterozygous mutant mice are characterized by an overall small body size, small eyes with coloboma, small or lacking lens with cataract, abnormal folding of the retina and reduction of the pigment layer. The anterior chamber is usually missing. Mutations in the Pax6 gene lead to an impairment of axonal growth and differentiation, and delay migration of preneuronal cells. Optic nerve cross-sectional area and fiber count are decreased in these mutant mice, but probably indirectly as a consequence of reduced neural retina size. Formation of lens and of nasal cavity placodes are dependent on normal Pax6 expression. | ||
| 002623 | C57BL/6JSmn-Dstncorn1-2J/J | Repository- Live |
| Histological assessment of corneas from mice homozygous for the Dstn corn1-2J mutation reveals focal epithelial thickening and enlarged surface epithelial cells with degenerating nuclei. These mice lack the neovascularization found in mice homozygous for the Dstn corn1 mutation and have a more mild corneal epithelial phenotype. Preliminary assessment indicates that this variation in phenotype results from the distinct mutations in Dstn, not from differences in genetic background. In both mutants the corneal epithelial cells show increased levels and altered organizational patterns of filamentous actin. In the Dstncorn1 mutants this alteration to filamentous actin has been shown to result in accelerated proliferation of basal corneal epithelial cells. (Smith et al., 1996; Wang et al., 2001; Ikeda et al., 2003.) | ||
| 001998 | CFW-Em/J | Repository- Live |
| 002026 | BALB/cHeA-Foxe3dyl/J | Repository-Cryopreserved |
Dysgenetic lens (Foxe3dyl) was originally characterized as an autosomal recessive mouse mutant but Foxe3 haploinsufficiency can also yield a similar phenotype characterized by defective lens development and cataracts. Homozygotes are viable and fertile. The most prominent abnormality is the irregular shape and reduced size of the lens. The pupil is also smaller and exhibits abnormal reactivity. The major morphological hallmark of homozygous Foxe3dyl mice is the persistent attachment of the lens to the corneal epithelium. The iris can also be fused with the lens but the retina remains unaffected. The lens contains fewer secondary fibers but when present, these fibers are very disorganized and the tissue contains large vacuoles. The developing lens initially forms properly as the lens placode is induced within the anterior neural ectoderm but around embryonic day 10 the mutant lens vesicle does not completely close and detach from the
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| 000316 | C3H/HeSn-Gpr161vl/J | Repository-Cryopreserved |
| 000942 | STOCK Pitx3ak/2J | Repository-Cryopreserved |
| Mice homozygous for the Pitx3ak mutation exhibit microphthalmia (small eyes) and aphakia (no lens) related to arrested lens development. The mesencephalic dopamine system is malformed and as a result homozygotes fail to develop dopaminergic neurons of the substantia nigra (Smidt et al., 2004). Homozygotes display sensorimotor deficits specific to the nigrostriatal pathway such as the challenge beam and pole test and the test for spontaneous exploratory activitiy in a cylinder. These deficits can be reversed by L-DOPA administration (Hwang et al., 2005). This mutant mouse strain may be useful in studies of Parkinson's disease. | ||
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