Analysis Tools|
Allele Symbol Allele Name Allele ID |
Fgfr1tm1.1Upir targeted mutation 1.1, Ulla Pirvola MGI:3529270 |
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| Summary |
3 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• phenotype is stated to be similar to that of Fgfr1tm1Jrt homozygotes; however, no data are presented in J:78879
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• the thickness of each band of cardiac actin is increased and average sarcomere thickness is increased to 1.01 um compared to 0.65 um in wild-type
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• at E12.5 the ventricular wall is thinner than normal
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• individual cardiomyoblasts appear larger and premature differentiation of cardiomyoblasts is seen
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• at E12.5 the atria are enlarged
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• severe hypoplasia is seen, however the patterning of the cardiac cushions, septum, and ventricular layers appears normal
• at E12.5 the heart does not fill the pericardial space
• hypoplasia is more severe and uniform than in Fgf9tm1Dor homozygotes
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• biventricular dilation is seen in newborn mutants
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• biventricular dilation is seen in newborn mutants
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• myocardial proliferation is decreased throughout the base and apex of both ventricles
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• the thickness of each band of cardiac actin is increased and average sarcomere thickness is increased to 1.01 um compared to 0.65 um in wild-type
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• at E12.5 the ventricular wall is thinner than normal
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• myocardial proliferation is decreased throughout the base and apex of both ventricles
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• myocardial proliferation is decreased throughout the base and apex of both ventricles
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mutants die within 24 hrs after birth
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• at birth, mutant cochleae are frequently slightly shorter than normal
• however, mutant otocysts appear morphologically normal at E10.5 and E11.5
• in addition, initiation of cochlear duct outgrowth from the otocyst is unaffected at E12.5
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• at birth, the sensory epithelium of the upper cochlear half is arranged in small sensory patches that mainly consist of IHCs and pillar supporting cells, while the lower cochlear half is less severely affected
• in contrast, the vestibular sensory epithelium remains unchanged
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• at around birth, the organ of Corti is severely disrupted due to impaired production of precursor cells between E12 and E15, as shown by BrdU labeling
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• at E16.5, mutants display no molecular signs of HC specification or differentiation in the gap regions found between sensory patches; OHCs are more severely affected
• at E16.5, the remaining HCs in the sensory patches appear to undergo normal differentiation
• at E18.5, most cochlear sections are devoid of HCs and the greater epithelial ridge is abnormally thin, due to reduced precursor cell proliferation in the ventral wall of the cochlear duct between E12 and E15.5
• apparently, the remaining precursors of the organ of Corti preferentially differentiate into IHCs and pillar cells
• no differences in precursor cell proliferation rate are observed in the dorsal, non-sensory wall of the cochlear duct
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• at P0, mutants show a 85% reduction in the total number of differentiating HCs relative to wild-type mice
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• at birth, only very low numbers of OHCs are formed, and these are located in lower cochlear half
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• at birth, the small sensory patches found in the upper cochlear half frequently show doublet IHCs instead of a single continuous IHC row
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• at birth, the small sensory patches found in the upper cochlear half frequently show an accumulation of disorientated IHCs at the edges
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• at birth, the sensory patches found in the upper cochlear half frequently show no signs of differentiation of supporting cells
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• at E16.5, mutants display no molecular signs of HC specification or differentiation in the gap regions found between sensory patches; OHCs are more severely affected
• at E16.5, the remaining HCs in the sensory patches appear to undergo normal differentiation
• at E18.5, most cochlear sections are devoid of HCs and the greater epithelial ridge is abnormally thin, due to reduced precursor cell proliferation in the ventral wall of the cochlear duct between E12 and E15.5
• apparently, the remaining precursors of the organ of Corti preferentially differentiate into IHCs and pillar cells
• no differences in precursor cell proliferation rate are observed in the dorsal, non-sensory wall of the cochlear duct
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• at P0, mutants show a 85% reduction in the total number of differentiating HCs relative to wild-type mice
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• at birth, only very low numbers of OHCs are formed, and these are located in lower cochlear half
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• at birth, the small sensory patches found in the upper cochlear half frequently show doublet IHCs instead of a single continuous IHC row
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• at birth, the small sensory patches found in the upper cochlear half frequently show an accumulation of disorientated IHCs at the edges
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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 11/19/2024 MGI 6.24 |
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