Phenotypes associated with this allele
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
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skeleton
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• by P30, limbs injected with adenovirus cre at P11 exhibit bony calluses encasing the tibia and fibula as well as fused with the pelvis and femur rendering hip, knee and ankle joints immobile unlike in similarly treated wild-type mice
• however, treatment of adenovirus cre exposed mice with LDN-193189, an inhibitor of BMP type I receptors, or dexamethasone reduces ectopic calcifications
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• by P30, limbs injected with adenovirus cre at P11 exhibit reduced mobility including loss of passive flexion in the hip, knee and ankle under aesthesia unlike in similarly treated wild-type mice
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muscle
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• regardless of LDN-193189 treatment, limbs injected with adenovirus cre at P11 exhibit mononuclear cell infiltration and myocyte edema in tissues undergoing recombination unlike in similarly treated wild-type mice
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immune system
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• regardless of LDN-193189 treatment, limbs injected with adenovirus cre at P11 exhibit mononuclear cell infiltration and myocyte edema in tissues undergoing recombination unlike in similarly treated wild-type mice
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-cre/Esr1*)5Amc mutation
(9 available)
Tg(CAG-LacZ,-ACVR1*,-EGFP)35-1Mis mutation
(0 available)
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skeleton
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N |
• unlike mice treated with adenoviral cre, tamoxifen treated mice exhibit normal ossification and joint mobility
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• tamoxifen treated mice injected with a control adenovirus exhibit decreased limb motion and small ectopic calcifications by P14
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muscle
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N |
• unlike mice treated with adenoviral cre, tamoxifen treated mice exhibit normal myocytes
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-LacZ,-ACVR1*,-EGFP)35-1Mis mutation
(0 available)
Tg(KRT14-cre)1Amc mutation
(2 available)
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mortality/aging
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• all newborn pups die within 24 h of birth
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behavior/neurological
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• all newborn pups lack milk in their stomachs
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craniofacial
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• the primary palate fails to fuse with the secondary palate
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• at E18.5, palatal shelves of the anterior secondary palate fail to fuse with each other and with the nasal septum
• in the middle part of the secondary palate, the fusion of mesenchymal tissue is impaired by the presence of an epithelial seam
• an epithelial cyst-like tissue is detected intermittently at the midline of hard palate and soft palate
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• although medial edge epithelium (MEE) seam formation is normal at E14.5, the MEE seam is not degraded at E15.5, unlike in control embryos
• TUNEL assays showed a significant reduction of apoptotic cells in MEE at E14.5; also, the expression level of cleaved caspase-3 is significantly reduced in MEE cells at E14.5
• downregulation of cell death is accompanied with upregulation of deltaNp63 in MEE at E14.5
• Ki67 staining showed a slight but significant increase of proliferating cells in MEE at E14.5 with continued ability of MEE cells to proliferate at E15.5
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• a white strip is found in the midline of the secondary palate including the soft palate
• however, cleft soft palate is not observed
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• at E18.5, fusion of palatal mesenchyme in the hard palate is hampered by epithelial tissue
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• at E18.5, fusion of muscle fibers in the soft palate is hampered by epithelial tissue
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• at E18.5, an epithelial cyst-like tissue prevents the fusion of the tensor veli palatini muscle in the soft palate
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• mice develop submucous cleft palate (SMCP) without cleft soft palate
• SMCP is caused by abnormal medial edge epithelium persistence
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digestive/alimentary system
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• the primary palate fails to fuse with the secondary palate
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• at E18.5, palatal shelves of the anterior secondary palate fail to fuse with each other and with the nasal septum
• in the middle part of the secondary palate, the fusion of mesenchymal tissue is impaired by the presence of an epithelial seam
• an epithelial cyst-like tissue is detected intermittently at the midline of hard palate and soft palate
|
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• although medial edge epithelium (MEE) seam formation is normal at E14.5, the MEE seam is not degraded at E15.5, unlike in control embryos
• TUNEL assays showed a significant reduction of apoptotic cells in MEE at E14.5; also, the expression level of cleaved caspase-3 is significantly reduced in MEE cells at E14.5
• downregulation of cell death is accompanied with upregulation of deltaNp63 in MEE at E14.5
• Ki67 staining showed a slight but significant increase of proliferating cells in MEE at E14.5 with continued ability of MEE cells to proliferate at E15.5
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• a white strip is found in the midline of the secondary palate including the soft palate
• however, cleft soft palate is not observed
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• at E18.5, fusion of palatal mesenchyme in the hard palate is hampered by epithelial tissue
|
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• at E18.5, fusion of muscle fibers in the soft palate is hampered by epithelial tissue
|
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• at E18.5, an epithelial cyst-like tissue prevents the fusion of the tensor veli palatini muscle in the soft palate
|
|
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• mice develop submucous cleft palate (SMCP) without cleft soft palate
• SMCP is caused by abnormal medial edge epithelium persistence
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growth/size/body
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• the primary palate fails to fuse with the secondary palate
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|
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• at E18.5, palatal shelves of the anterior secondary palate fail to fuse with each other and with the nasal septum
• in the middle part of the secondary palate, the fusion of mesenchymal tissue is impaired by the presence of an epithelial seam
• an epithelial cyst-like tissue is detected intermittently at the midline of hard palate and soft palate
|
|
|
• although medial edge epithelium (MEE) seam formation is normal at E14.5, the MEE seam is not degraded at E15.5, unlike in control embryos
• TUNEL assays showed a significant reduction of apoptotic cells in MEE at E14.5; also, the expression level of cleaved caspase-3 is significantly reduced in MEE cells at E14.5
• downregulation of cell death is accompanied with upregulation of deltaNp63 in MEE at E14.5
• Ki67 staining showed a slight but significant increase of proliferating cells in MEE at E14.5 with continued ability of MEE cells to proliferate at E15.5
|
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• a white strip is found in the midline of the secondary palate including the soft palate
• however, cleft soft palate is not observed
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• at E18.5, fusion of palatal mesenchyme in the hard palate is hampered by epithelial tissue
|
|
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• at E18.5, fusion of muscle fibers in the soft palate is hampered by epithelial tissue
|
|
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• at E18.5, an epithelial cyst-like tissue prevents the fusion of the tensor veli palatini muscle in the soft palate
|
|
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• mice develop submucous cleft palate (SMCP) without cleft soft palate
• SMCP is caused by abnormal medial edge epithelium persistence
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muscle
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• at E18.5, fusion of muscle fibers in the soft palate is hampered by epithelial tissue
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• at E18.5, an epithelial cyst-like tissue prevents the fusion of the tensor veli palatini muscle in the soft palate
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Analysis Tools