Search Criteria: Research Area is "Sensorineural Research: Cataracts"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 001801 | C57BL/10ScSn-Dmdmdx/J | Level 3 |
| The X-linked dystrophin gene (Dmd) is highly expressed in muscle cells and encodes a cytoskeletal protein which localizes to the inner face of the sarcolemma. Dystrophin molecules bind to cytoskeletal F-actin and transmembrane beta-dystroglycan as part of a complex, multimolecular unit that mediates signaling between the intracellular cytoskeleton and the extracellular matrix. The structure and localization also suggest that dystrophin is important for stabilizing the plasma membrane, particularly during contraction. The mdx mutation of Dmd is recessive and heterozygous females are visually indistinguishable from wild-type mice. Females homozygous and males hemizygous for the Dmdmdx allele retain a normal lifespan and can survive up to two years. Like human patients who suffer from one of the most common neuromuscular diseases, Duchenne muscular dystrophy (DMD), the Dmdmdx mutants do not express dystrophin and therefore have been ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 ..... | ||
| 006233 | B6.129S1-Casp3tm1Flv/J | Repository- Live |
| On this C57BL/6 congenic background, homozygotes are viable, fertile, and reach adulthood, but females reported display suboptimal mothering instincts. Functional endogenous protein and mRNA are absent from all tissues tested. Homozygous mice are resistant to in vivo cerebral ischemia/reperfusion and in vitro oxygen-glucose deprivation. Ovaries from female homozygotes show aberrant atretic follicles associated with a granulosa cell-intrinsic defect in apoptosis as well as defective corpus luteum regression. Homozygous mice are congenitally deaf with hair cell defects in the Organ of Corti. Optic lens formation/morphology also is abnormal with cataracts at the anterior lens pole. Of note, these mice lack the embryonic/perinatal-lethal brain pathology observed in mutant mice on the 129 and mixed B6;129 genetic backgrounds. These mutant mice may be useful in studies of apoptosis, ovarian follicle and corpus luteum development, and eye and ear development. | ||
| 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. | ||
| 001923 | B6EiC3Sn a/A-Ts(417)2Lws TimT(4;17)3Lws/J | Repository- Live |
| The Tim mutation (translocation induced circling mutation) was induced by ethylene oxide in a mutagenesis experiment. The mutation was induced simultaneously with a reciprocal translocation between Chrs 4 and 17. Because the mutation has so far been inseparable from the translocation, it may be that one of the translocation breakpoints has disrupted a gene on Chr 4 or 17. Heterozygotes exhibit circling, head tossing, poor limb coordination, and corneal clouding. The affected mice are usually smaller than wildtype littermates. Inner ear studies have not been done. The mutants swim poorly but can orient themselves in the water. One mutated copy of the gene is dominant over two normal alleles because segmentally trisomic mice with two normal Chrs 4 and 17 and the small 417 translocation product have the behavioral abnormalitites. Breeding is generally poor. | ||
| 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 |
| 003148 | STOCK chky/J | Repository- Live |
| Mice homozygous for the chick yellow mutation on an albino background have a pale yellow coat color evident by approximately 10 days of age when the first coat of hair comes in. Cataracts, lens extrusion, and retinal degeneration develop. Independent of the chick yellow mutation, mice of this background, which is an inbred of an ICR outbred population, may develop polydipsia with age. | ||
| 000385 | 129S;AKR-bs/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the spontaneous blind sterile mutation (bs) are characterized by bilateral nuclear cataracts, smaller than normal eyes, and glossy coats. Female mutant mice are fertile but males are sterile. Cataracts are visible in 16 day embryos and continue to adulthood. Adult male mice copulate normally but have smaller than normal testes. Defects in spermatogenesis lead to a reduced number of sperm and those that are formed completely lack acrosomes. | ||
| 005624 | B6(V) Lepob-whe/GrsrJ | Cryopreserved - Ready for recovery |
| White eye homozygotes have partially or completely open eyelids at two days of age. Subsequently, likely as a consequence of infection, homozygotes develop a small white spot and atypical growth of blood vessels on the cornea of each eye, although occassionally only one eye is affected. | ||
| 004276 | B6.129-Figntm1Frk/Frk | Cryopreserved - Ready for recovery |
| 000026 | B6.C3-Gli3Xt-J/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the extra toes-J spontaneous mutation (Gli3Xt-J) have varying numbers of extra digits on preaxial side of feet. Homozygous mutant mice die in utero with multiple abnormalities. Excessively large pharyngeal arches and an open neural tube are evident at E9. Homologous to Grieg's cephalopoly-syndactyly, a rare multi-system syndrome in humans. | ||
| 004275 | B6.Cg-Fignfi/Frk | Cryopreserved - Ready for recovery |
| 002201 | B6;129-Gja1tm1Kdr/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Gja1tm1Kdr targeted mutation die at birth. The cause of death is a failure in pulmonary gas exchange caused by a swelling and blockage of the right ventricular outflow tract from the heart. The cardiac abnormality involves a delay in the normal looping of the ascending limb of the heart tube, which includes the right ventricle and the outflow tract. This predisposes homozygous mutant mice to malformations of the subpulmonary outflow tract and tricuspid valve. The mutation also predisposes mice to lens cataracts and causes a severe reduction of germ cell numbers in homozygous mutant mice of both sexes. Both neonatal and adult mice heterozygous for the Gja1tm1Kdr targeted mutation have slower ventricular epicardial conduction of paced beats in the heart. | ||
| 005043 | B6;129-nmf166/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the nmf166 mutation have lens extrusion cataracts and deep anterior chambers at 12 weeks of age. View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf166 entry. | ||
| 003728 | B6;129S-Sparctm1Hwe/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for Sparc are viable and fertile. They display decreased physical activity when handled but otherwise appear normal. Sparc transcripts and protein products are not detected in these animals. The development of cataracts and osteopenia are the predominant phenotypes. Lenticular opacity starts to develop at 1 to 2 months after birth, progressing to mature cataracts by 5-8 months of age. Intracellular vacuoles are apparent at 1-2 months, leading to a disruption of fiber cell packing. In later stages, the lens capsule ruptures and displacement of lens material into the anterior chamber is evident. At 17 weeks of age, null mice exhibit 50% less trabecular bone than that found in wild type controls. The loss is 70% at 36 weeks. Decreases in both osteoclast and osteoblast numbers are observed, the cumulative effect of which is a negative bone-balance leading to profound osteopenia. | ||
| 001280 | B6C3Fe a/a-Lse/J | Cryopreserved - Ready for recovery |
| Lse/+ pups can be identified at birth by the presence of an open auditory meatus, which in normal mice remains closed until approximately day 13, when the eyes also open. Fewer than the expected 50% affected pups are born, and about 50% of pups identified as Lse/+ fail to survive until weaning. Homozygotes either die prenatally or are indistinguishable from heterozygotes. The ears of Lse/+ mice are positioned lower and further forward than those of normal mice and are abnormally formed. These mice are not deaf. In addition to the ear abnormalities, Lse/+ mice are smaller than their normal littermates and have opaque corneas (Theiler and Sweet 1986). | ||
| 002026 | BALB/cHeA-Foxe3dyl/J | Cryopreserved - Ready for recovery |
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 ..... | ||
| 002000 | C3.Cg-CrygeElo/J | Cryopreserved - Ready for recovery |
| Heterozygotes and homozygotes have microphthalmia with normal ocular structures except for the lens. Homozygotes are viable and fertile. At embryonic day 12 there is poor elongation of the basal cytoplasm of the central lens fibers and the lens cavity remains open. At embryonic day 13 the elongation of the lens fiber and the convex nuclear arrangement shows poor progression, the central lens fibers are deranged, and the lens fibers are detached from the capsule at the basal surface. At birth the lens is approximately half the normal size and is deformed, with the lens cavity remaining open. In heterozygotes and homozygotes the lens degenerates by 30 days of age. | ||
| 000316 | C3H/HeSn-Gpr161vl/J | Cryopreserved - Ready for recovery |
| 001434 | C3HeB/FeJ x STX/Le-Mc1rE-so Gli3Xt-J Tw/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the twirler mutation (Tw) display head-shaking and circling behavior but are not deaf. There are morphological abnormalities of the inner ear which consist of irregularities in the outline of the semicircular canals, sometimes amounting to branching, and reduction or absence of otoliths. Moderate astrocytosis in the vestibular nuclei and cerebellar white matter has been reported. Homozygotes have cleft lip and palate or cleft palate only. They die within 24 hours after birth. Viability and fertility are normal except that adults tend to become obese and may then become sterile. Penetrance is incomplete. This strain is also carrying the sombre (Mc1rE-so) and extra toes-Jackson (Gli3St-J) mutations. Extra toes-J heterozygotes have varying numbers of extra digits on preaxial side of feet. Homozygotes die in utero with multiple abnormalities. Excessively large pharyngeal arches and an open neural tube are evident at E ..... For more information please see the full phenotype on the strain data sheet | ||
| 001533 | C3HeB/FeJ-Mc1rE-so Gli3Xt-J/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the extra toes-J spontaneous mutation (Gli3Xt-J) have varying numbers of extra digits on preaxial side of feet. Homozygous mutant mice die in utero with multiple abnormalities. Excessively large pharyngeal arches and an open neural tube are evident at E9. Homologous to Grieg's cephalopoly-syndactyly, a rare multi-system syndrome in humans. This strain is homozygous for the sombre mutation (Mc1rE-so). | ||
| 005006 | C57BL/6J-nmf131/J | Cryopreserved - Ready for recovery |
| Homozygosity for the nm131 mutation can cause retinal dysplasia, retinal degeneration, vitreal fibroplasia, and, less commonly, cataracts or microphthalmia. This mutation has low penetrance. View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf131 entry. | ||
| 001490 | C;AK-Gja8Lop10/J | Cryopreserved - Ready for recovery |
| The lens opacity 10 mutation in Gja8 is semidominant. Homozygotes are microphthalmic with foamy cataract of the entire lens apparent when the eyes open at 12 days of age and increasing in opaqueness with age. Bladder cells are found adjacent to the anterior and posterior subcapsular regions of the lens before birth, the lens nucleus begins to liquefy by 4 days of age and ruptures posteriorly, then the lens capsule thickens. Gja8Lop10 Heterozygotes are not microphthalmic and the phenotype associated with the mutation varies according to the genetic background. A nuclear haze or snowflake nuclear opacity is found in F1 heterozygotes of some backgrounds while a more severe dense nuclear opacity is evident by 4 weeks of age in F1 heterozygotes of other backgrounds including AKR/J and BALB/cJ. Mice homozygous for the Gja8tm1Paul targeted mutation, a recessive mutation in which the entire coding region is removed, do not display posterior lens r ..... For more information please see the full phenotype on the strain data sheet | ||
| 002489 | CBA/CaGnLe-Cryaalop18/J | Cryopreserved - Ready for recovery |
| Mice homozygous for Cryaalop18 develop large, dense nuclear cataracts. At embryonic day (E) 10 the lens vesicle in these homozygotes buds out from the surface ectoderm. At E14 tiny vacuoles develop in the lens, these are larger at E16, and by four months of age there is advanced degeneration of the cortex with posterior migration of the lens epithelial nuclei and the posterior pole of the lens shows abnormal lens fibers. However, the cataracts were not found to progress further after this age. (Chang et al., 1996.) | ||
| 002456 | FVB/N-Tg(CryHIVPR)72Gjj/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the expression of HIV-1 protease (HIVPr) linked to the lens alphaA-crystallin promoter are viable and fertile. Homozygotes develop bilateral cataracts at 23 - 24 days of age, beginning in the perinuclear region of the lens. Proteolysis begins with the loss of betaB1-, betaB3- and betaA3-crystallins and the appearance of crystallin fragments, accompanied by protein leakage and breakdown of cytoskeletal elements. It appears that the HIV-1 protease works in concert with other endogenous proteases to induce the changes that eventually result in opacification of the lens. | ||
| 000265 | MY/HuLeJ | Cryopreserved - Ready for recovery |
| 001646 | STOCK CrygdLop12/J | Cryopreserved - Ready for recovery |
| 002352 | STOCK MipCat-Fr/J | Cryopreserved - Ready for recovery |
| 000942 | STOCK Pitx3ak/2J | Cryopreserved - Ready for recovery |
| 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. | ||
| 001385 | STOCK lop13/J | Cryopreserved - Ready for recovery |
| lop13 is a recessive mutation that causes bilateral cataracts that do not affect the cortex of the lens. This presents at 3 to 4 weeks of age as a white area in the center of the lens. The size of the eyes is normal. (Varnum, 1981.) | ||
| 000312 | STOCK stb + a/+ Fignfi a/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the fidget spontaneous mutation (Fignfi) toss their heads from side to side and tend to run in circles. Homozygous fidgit mice are hypersensitive to sound in early life, but later lose hearing ability. Corneal lesions are common, and hind foot polydactylism occurs. The bony labyrinth is quite defective. Other abnormalities including small eyes, absence of lachrymal glands, dislocation of the hip, and displaced parafloccular lobes of the cerebellum. Viability of homozygotes is usually less than normal and fertility is poor. The STOCK is also carrying the stubby spontaneous mutation (stb). Homozygous stubby mice are recognizable at 4 or 5 days by a domed head and thick short tail. Adult stubby mice have shorter heads, bodies, and legs compared to wildtype mice. Most females are fertile but males do not breed. Male mice do produce normal numbers of motile sperm. Cartilage histology is within normal limits, but chondrogenesis stops earlier than ..... For more information please see the full phenotype on the strain data sheet | ||
| 001032 | STOCK In(1)38Rk/J | Cryopreserved - Ready for recovery |
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