Analysis Tools|
Allele Symbol Allele Name Allele ID |
Fgf8+ wild type MGI:2432618 |
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| Summary |
17 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• Background Sensitivity: fewer than expected are found at weaning unlike when mice are on a CD-1 outbred background
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• mice tend to have a lower body weight
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Fgf8tm1Moon/Fgf8+ Six1tm1(cre)Xli/Six1+ newborns exhibit interrupted aortic arch-type B and vascular ring
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• 83% display great vessel defects like cervical aortic arch or interrupted aortic arch type B
• embryos have severely hypoplastic proximal and distal outflow tract cushions compared to wild-type controls
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• defects are seen in 78% of fetuses at E18.5 when tamoxifen is administered at E8.5
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• defects are seen in 52, 32, and 63% of fetuses at E18.5 when tamoxifen is administered at E7.5, 8.5 or 9.5 respectively
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• ~16% of double heterozygotes exhibit PAA-related cardiovascular defects vs 0% in single Gbx2tm1Mrt or Fgf8tm1.4Mrt heterozygotes
• however, no incidences of a double outlet right ventricle, an overriding aorta or a retroesophageal right subclavian artery are observed
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• 20% of double heterozygotes with cardiovascular defects display a retroesophageal right subclavian artery
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• 80% of double heterozygotes with cardiovascular defects exhibit a right aortic arch
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• ~16% of double heterozygotes exhibit PAA-related cardiovascular defects vs 0% in single Gbx2tm1Mrt or Fgf8tm1.4Mrt heterozygotes
• however, no incidences of a double outlet right ventricle, an overriding aorta or a retroesophageal right subclavian artery are observed
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• ~16% of double heterozygotes exhibit PAA-related cardiovascular defects vs 0% in single Gbx2tm1Mrt or Fgf8tm1.4Mrt heterozygotes
• however, no incidences of a double outlet right ventricle, an overriding aorta or a retroesophageal right subclavian artery are observed
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mutant mice exhibit a significantly increased frequency, but not severity, of PAA-related cardiovascular defects relative to single Gbx2tm1Mrt homozygotes (86% vs 39%, respectively)
• however, no incidences of a double outlet right ventricle or an overriding aorta are observed
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• 16.6% of mutant mice with cardiovascular defects exhibit a retroesophageal right subclavian artery vs 21% of single Gbx2tm1Mrt homozygotes
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• 25% of mutant mice with cardiovascular defects exhibit an interrupted aortic arch (IAA) type B vs 26% of single Gbx2tm1Mrt homozygotes
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• 58.3% of mutant mice with cardiovascular defects exhibit a right aortic arch (RAA) vs 37% of single Gbx2tm1Mrt homozygotes
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• ~29% of mutant mice exhibit abnormal thymus development, either as a single-lobed thymus or as an overall reduction in thymus size (not observed in single Gbx2tm1Mrt homozygotes or Fgf8tm1.4Mrt heterozygotes)
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• ~29% of mutant mice exhibit abnormal thymus development, either as a single-lobed thymus or as an overall reduction in thymus size (not observed in single Gbx2tm1Mrt homozygotes or Fgf8tm1.4Mrt heterozygotes)
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• mutant mice exhibit a significantly increased frequency, but not severity, of PAA-related cardiovascular defects relative to single Gbx2tm1Mrt homozygotes (86% vs 39%, respectively)
• however, no incidences of a double outlet right ventricle or an overriding aorta are observed
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• a few mutant mice display a reduced mandible
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• a few mutant mice exhibit small external ears
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• a few mutant mice exhibit small external ears
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• a few mutant mice display a reduced mandible
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• mutant mice exhibit a significantly increased frequency, but not severity, of PAA-related cardiovascular defects relative to single Gbx2tm1Mrt homozygotes (86% vs 39%, respectively)
• however, no incidences of a double outlet right ventricle or an overriding aorta are observed
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• at E9.5, mutant mice display a NCC migratory patterning defect similar to that of single Gbx2tm1Mrt homozygotes
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• at E9.5, mutant mice display a NCC migratory patterning defect similar to that of single Gbx2tm1Mrt homozygotes
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• ~29% of mutant mice exhibit abnormal thymus development, either as a single-lobed thymus or as an overall reduction in thymus size (not observed in single Gbx2tm1Mrt homozygotes or Fgf8tm1.4Mrt heterozygotes)
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• a few mutant mice exhibit small external ears
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in 26% of mice
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• in 26% of mice
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• in 26% of mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• cerebellar vermis aplasia present at birth
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• due to cerebellar vermis aplasia
• cerebellar hemispheres are similar in size to controls
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• increased ABR threshold at all test frequencies
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• increased ABR threshold at all test frequencies
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• despite expected Mendelian ratios at E9.5 to E10.5, fewer than expected mice are present at E18.5
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• at E9.5 to E10.5
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• deletion of midbrain/cerebellum structures
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• at E9.5 to E10.5
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• strong
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• at E9.5 to E10.5
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• at E9.5 to E10.5
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• the nasal pits are somewhat larger and are angled slightly downwards toward the maxilla
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• slight widening of the midface
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• 8 of 18 mice exhibit a unilateral premaxillary fusion defect resulting in a unilateral cleft primary palate
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• 8 of 18 mice exhibit a unilateral premaxillary fusion defect resulting in a unilateral cleft primary palate
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• slight widening of the midface
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• 8 of 18 mice exhibit a unilateral premaxillary fusion defect resulting in a unilateral cleft primary palate
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• the nasal pits are somewhat larger and are angled slightly downwards toward the maxilla
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tissue losses in inferior colliculus
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• Purkinje cell migration begins earlier than normal
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• overall size of vermis about 76% of control size but hemispheres normal
• decreased cell proliferation in vermis by E11.5
• neuroepithelium thinner than normal
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• lobe III of the vermis is lost by age 2 days and in adults
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• asymmetrical gait seen in about 20% of mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• cerebellum has begun to foliate at birth
• granule layer extends along the anterior posterior length of the cerebellum
• isthmus is formed
• Purkinje cells are normal
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• not clearly distinguishable
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• all aortic arch patterning defects observed at E18.5 are attributable to a failure of the fourth pharyngeal arch artery (PAA) development evident at E10.5; the third and sixth PAAs appear normal
• the number of arteries scored as non-patent to ink (i.e. 'absent' fourth PAA) are significantly higher in double heterozygotes than in embryos heterozygous for Tbx1tm1Bld alone
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• at E18.5, 18 out of 36 (50%) of double heterozygotes exhibit aortic arch patterning defects vs 27% of mice heterozygous for Tbx1tm1Bld alone
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• three show A-RSA associated with a cervical aortic arch
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• eight of these 18 double heterozygotes exhibit interruption of the aortic arch type B (IAA-B, occurring between the left common carotid artery and the left subclavian artery) associated with a right aortic arch (RAA)
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• eight of these 18 double heterozygotes exhibit interruption of the aortic arch type B (IAA-B, occurring between the left common carotid artery and the left subclavian artery) associated with a right aortic arch (RAA)
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• at E18.5, 14 of 30 double heterozygotes exhibit thymic hypoplasia and/or lobe asymmetry
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• all aortic arch patterning defects observed at E18.5 are attributable to a failure of the fourth pharyngeal arch artery (PAA) development evident at E10.5; the third and sixth PAAs appear normal
• the number of arteries scored as non-patent to ink (i.e. 'absent' fourth PAA) are significantly higher in double heterozygotes than in embryos heterozygous for Tbx1tm1Bld alone
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• all aortic arch patterning defects observed at E18.5 are attributable to a failure of the fourth pharyngeal arch artery (PAA) development evident at E10.5; the third and sixth PAAs appear normal
• the number of arteries scored as non-patent to ink (i.e. 'absent' fourth PAA) are significantly higher in double heterozygotes than in embryos heterozygous for Tbx1tm1Bld alone
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• at E18.5, 14 of 30 double heterozygotes exhibit thymic hypoplasia and/or lobe asymmetry
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• at E18.5, 14 of 30 double heterozygotes exhibit thymic hypoplasia and/or lobe asymmetry
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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 03/25/2025 MGI 6.24 |
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