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• mice exhibit increased apoptosis in the epidermis compared to wild-type mice
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Allele Symbol Allele Name Allele ID |
Ctnna1tm1Efu targeted mutation 1, Elaine Fuchs MGI:2677796 |
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| Summary |
9 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice exhibit increased apoptosis in the epidermis compared to wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• slower growth of horizontal blood vessels in retina at age P7 after tamoxifen administration from age P1-P4
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• increased blood vessel leakage in retina at age P7 after tamoxifen administration from age P1-P4
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• slower growth of horizontal blood vessels in retina at age P7 after tamoxifen administration from age P1-P4
• increased blood vessel leakage at age P7 after tamoxifen administration from age P1-P4
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| exudative vitreoretinopathy | DOID:0050535 |
OMIM:PS133780 |
J:328283 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• slower growth of horizontal blood vessels in retina at age P3 during tamoxifen administration from age P1-P4
• slower growth of horizontal blood vessels in retina at age P9 after tamoxifen administration from age P1-P4
• delayed growth of vertical blood vessels in superficial retina vascular plexus at age P9 after tamoxifen administration from age P1-P
• lack of vertical secondary and tertiary vessels in retina at age P9 after tamoxifen administration from age P1-P4
• defects of vascular growth into deeper layers of retina at age P9 after tamoxifen administration from age P1-P4
• defects in periphery of superficial retina vascular plexus at age P13 after tamoxifen administration from age P6
• fewer vessels in retina OPL and minimal vessels in retina IPL at age P13 after tamoxifen administration from age P6
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• enlarged superficial vessels in retina at age P9 after tamoxifen administration from age P1-P4
• enlarged blood vessels in brain at age P9 after tamoxifen administration from age P1-P4
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• in eyes after tamoxifen administration from age P1-P4
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• extensive blood leakage in brain at age P9 after tamoxifen administration from age P1-P4
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• slower growth of horizontal blood vessels at age P3 during tamoxifen administration from age P1-P4
• slower growth of horizontal blood vessels and enlarged superficial vessels at age P9 after tamoxifen administration from age P1-P4
• delayed growth of vertical blood vessels in superficial retina vascular plexus at age P9 after tamoxifen administration from age P1-P4
• lack of vertical secondary and tertiary vessels at age P9 after tamoxifen administration from age P1-P4
• defects of vascular growth into deeper layers at age P9 after tamoxifen administration from age P1-P4
• defects in periphery of superficial retina vascular plexus at age P13 after tamoxifen administration from age P6
• fewer vessels in OPL and minimal vessels in IPL at age P13 after tamoxifen administration from age P6
• increased blood vessel leakage at age P9 after tamoxifen administration from age P1-P4
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• slower regression after tamoxifen administration from age P1-P4
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• after tamoxifen administration from age P1-P4
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• most mice die by age P9 after tamoxifen administration from age P1-P4
• mice die by age P13-P14 after tamoxifen administration from age P6
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• extensive blood leakage in brain at age P9 after tamoxifen administration from age P1-P4
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• after tamoxifen administration from age P1-P4
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• after tamoxifen administration from age P1-P4
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| exudative vitreoretinopathy | DOID:0050535 |
OMIM:PS133780 |
J:328283 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice exhibit minimal effects on prenatal skeletal development
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• at E15, mice exhibit a delay in chondrocyte hypertrophy
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• at E18.5, ossification in the skull is slightly delayed
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice have severe intracellular adhesion defects
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• in culture, keratinocytes overgrow the monolayer, grow faster than wild-type cells, do not require a feeder layer, are more sensitive to growth factors, and have an increased ability to breakdown matrix
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• limbs fail to develop completely
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• in culture, keratinocytes overgrow the monolayer, grow faster than wild-type cells, do not require a feeder layer, are more sensitive to growth factors, and have an increased ability to breakdown matrix
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• mice have diminished signs of hair follicle development
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• epidermal-dermal boundary was difficult to discern
• clumps of keratinocytes with morphology and differentiation characteristic of epidermis and not hair follicles and that are devoid of surface epidermis are present within the dermis
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• large sections of the epidermis are missing
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• epidermis is thick and disorganized, particularly within the basal cell layer
• basal cells are round and spinous
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• keratinocytes are frequently binucleated and unusually large
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• visible peeling occurs
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• epidermis is thick and disorganized, particularly within the basal cell layer
• epidermal-dermal boundary was difficult to discern
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice die between 2 and 3 weeks after birth
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• apical-junctional complexes and cell polarity is lost in neuronal progenitor cells
• some cells are non-polarized, round and loosely connected to each other
• at E13.5, neuronal progenitor cells have shorter cell cycles
• however, treatment with cyclopamine rescues normal cell cycling
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• mice brains are dysplastic
• ventricular cells are scattered throughout the developing brain forming invasive tumor-like masses that displayed widespread pseudopalisading and the formation of rosettes
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• starting at E13.5, embryonic brains are hyperplastic with twice as many cells at birth compared to in wild-type brains
• however, hyperplasia can be reversed by treating embryos with cyclopamine
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• brain weight and brain-weight-relative-to-body-weight are increased
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• the lateral ventricle is shifted posteriorly and ventrally
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• at E13.5, size and thickness of the cortex is increased
• apoptosis in the cortex is reduced by half
• however, treatment with cyclopamine rescues increased apoptosis rates
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• mice are born with enlarged heads
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• despite mice having large heads that continue to grow, their bodies exhibit growth retardation
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• at E13.5, neuronal progenitor cells have shorter cell cycles
• however, treatment with cyclopamine rescues normal cell cycling
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• apical-junctional complexes and cell polarity is lost in neuronal progenitor cells
• some cells are non-polarized, round and loosely connected to each other
• at E13.5, neuronal progenitor cells have shorter cell cycles
• however, treatment with cyclopamine rescues normal cell cycling
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• pups with homozygous mothers weight 50% of normal mice
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• pups with homozygous mothers fail to thrive
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• mammary glands have reduced numbers of epithelial cells
• some epithelial cells remain condensed and disorganized without forming alveolar structures
• lumens are absent from clusters of epithelium
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• milk proteins are reduced
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• apoptosis in mammary epithelium is increased
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• mammary glands have reduced numbers of epithelial cells
• some epithelial cells remain condensed and disorganized without forming alveolar structures
• lumens are absent from clusters of epithelium
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• milk proteins are reduced
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• apoptosis in mammary epithelium is increased
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• pups with homozygous mothers fail to thrive, are about 50% of normal weight and some do not survive lactation
• in litters that experience lethality, the litters are reduced to 50% at day 5 and 25% by day 10
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mammary glands have reduced numbers of epithelial cells
• some epithelial cells remain condensed and disorganized without forming alveolar structures
• lumens are absent from clusters of epithelium
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• milk proteins are reduced
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• apoptosis in mammary epithelium is increased
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• apoptosis in mammary epithelium is increased
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• mammary glands have reduced numbers of epithelial cells
• some epithelial cells remain condensed and disorganized without forming alveolar structures
• lumens are absent from clusters of epithelium
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• milk proteins are reduced
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• apoptosis in mammary epithelium is increased
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• apoptosis in mammary epithelium is increased
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• occasionally hair development is not on schedule
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• progressive 8 months after tamoxifen treatment
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• progressive 8 months after tamoxifen treatment
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 04/30/2024 MGI 6.23 |
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