Analysis Tools|
Allele Symbol Allele Name Allele ID |
Tfap2atm1(cre)Moon targeted mutation 1, Anne M Moon MGI:2686837 |
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| Summary |
9 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Effects of Cre-mediated rescue of Chd7Gt(XK403)Byg mutation on the arch artery phenotype at E10.5
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Fourth pharyngeal arch artery aplasia in Tbx1tm2.1Bem/Tbx1+ Tfap2atm1(cre)Moon/Tfap2a+ mice
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• at E10.5, 76% of mice exhibit hypoplasia of the fourth pharyngeal aortic arch
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• at E10.5, 76% of mice exhibit hypoplasia of the fourth pharyngeal aortic arch
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• at E10.5, 76% of mice exhibit hypoplasia of the fourth pharyngeal aortic arch
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in 9 of 20 mice
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• at E15.5, 11 of 20 mice exhibit aberrant right subclavian artery unlike wild-type mice
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• mice exhibit defects in the great vessels unlike wild-type mice
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• one mouse exhibits truncus arteriosus communis unlike wild-type mice
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• at E15.5 in one mouse
• at E18.5 in one mouse
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• in 9 of 20 mice
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• 12 of 20 mice exhibit an absent or hypoplastic thymus unlike wild-type mice
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• in 9 of 20 mice
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• 12 of 20 mice exhibit an absent or hypoplastic thymus unlike wild-type mice
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• 12 of 20 mice exhibit an absent or hypoplastic thymus unlike wild-type mice
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• in 9 of 20 mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• disorganized tongue muscle fibers at E14
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• die around the time of birth
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• poor colonization of the outflow tract by cardiac neural crest cells at E10.5
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• poor colonization of the outflow tract by cardiac neural crest cells at E10.5
• at E11 the outflow tract has a lower density of cardiac neural crest cells and these cells are disorganized
• however, septation occurs normally
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• in some embryos
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• malformed outflow tract valves in 90% of mice at E12
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• poor colonization of the outflow tract by cardiac neural crest cells at E10.5
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• smaller and misshapen
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• less affected compared to germline null mice
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• at E17
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• fail to grow and close over the eye bulb at E17
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• boundary of ossification is abnormal
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• severely malformed
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• poorly developed
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• severely malformed palatal cartilage in 33% of mice with less severe malformations in the remaining 67% of mice
• otic capsule cartilage is absent at E16 in 33% of mice and reduced in 66% of mice
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• cartilage is absent at E16 in 33% of mice and reduced in 66% of mice
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• boundary of ossification is abnormal
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• severely malformed
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• poorly developed
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• severely malformed cartilage in 33% of mice with less severe malformations in the remaining 67% of mice
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• disorganized tongue muscle fibers at E14
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• small tongue at E14
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• severely malformed cartilage in 33% of mice with less severe malformations in the remaining 67% of mice
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• disorganized tongue muscle fibers at E14
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• small tongue at E14
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• severely malformed cartilage in 33% of mice with less severe malformations in the remaining 67% of mice
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• disorganized tongue muscle fibers at E14
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• small tongue at E14
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• poor colonization of the outflow tract by cardiac neural crest cells at E10.5
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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 |
| N |
• no behavioral abnormalities are seen
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• the average number of motor neurons is significantly reduced in mutants compared to wild-type mice although not to the same extent as in compound heterozygous mutants carrying Tg(Wnt1-cre)11Rth
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at E9.5, lens induction is abnormal as indicated by reduced Pax6+ cells
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• at E12.5, lens reduction is more severe than any other conditional cross but not as severe as in the Pygo2 null homozygotes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• those that survive to birth die postnatally due to lethal vascular defects in 30% and severe craniofacial defects in 100% of mutants
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• 25% die prior to birth
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• 30% show lethal vascular defects
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• 95% have abnormal fourth pharyngeal arch artery formation at E10.5
• migration and early differentiation of the 4th pharyngeal arch artery endothelial cells occurs normally but subsequent vascular organization fails such that at the 35-37 somite stage, endothelial cells remain disorganized and fail to form primitive vascular tubes, long after this vessel is patent and pericyte recruitment is under way in controls
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• 33% display bilateral aplasia of the fourth and sixth pharyngeal arch arteries at E10.5
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• 12% show bilateral hypoplasia of the 4th pharyngeal arch arteries
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• 33% display bilateral aplasia of the fourth and sixth pharyngeal arch arteries at E10.5
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• exhibit an abnormally large third pharyngeal arch artery
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• 30% of E18.5 mutants have interrupted aortic arch type B (IAAB)
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• 13% exhibit circumflex right aortic arch (RAA) or RAA with right ductus arteriosus
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• 46% exhibit coronary artery anomalies, in isolation or associated with other vascular defects
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• subclavian artery anomalies
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• 80% exhibit retroesophageal right subclavian artery or abnormal subclavian branching associated with other defects
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• 100% show severe craniofacial malformations
|
|
• 95% have abnormal fourth pharyngeal arch artery formation at E10.5
• migration and early differentiation of the 4th pharyngeal arch artery endothelial cells occurs normally but subsequent vascular organization fails such that at the 35-37 somite stage, endothelial cells remain disorganized and fail to form primitive vascular tubes, long after this vessel is patent and pericyte recruitment is under way in controls
|
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• 33% display bilateral aplasia of the fourth and sixth pharyngeal arch arteries at E10.5
|
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• 12% show bilateral hypoplasia of the 4th pharyngeal arch arteries
|
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• 33% display bilateral aplasia of the fourth and sixth pharyngeal arch arteries at E10.5
|
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• exhibit an abnormally large third pharyngeal arch artery
|
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• exhibit severe pharyngeal arch 1 hypoplasia and hypoplasia and fusion of the more caudal pharyngeal arches as early as E9.5
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• 95% have abnormal fourth pharyngeal arch artery formation at E10.5
• migration and early differentiation of the 4th pharyngeal arch artery endothelial cells occurs normally but subsequent vascular organization fails such that at the 35-37 somite stage, endothelial cells remain disorganized and fail to form primitive vascular tubes, long after this vessel is patent and pericyte recruitment is under way in controls
|
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• 33% display bilateral aplasia of the fourth and sixth pharyngeal arch arteries at E10.5
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• 12% show bilateral hypoplasia of the 4th pharyngeal arch arteries
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• 33% display bilateral aplasia of the fourth and sixth pharyngeal arch arteries at E10.5
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• exhibit an abnormally large third pharyngeal arch artery
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• exhibit an increase in apoptosis of neural crest cells migrating from rhombomeres 6-8
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• exhibit severe pharyngeal arch 1 hypoplasia and hypoplasia and fusion of the more caudal pharyngeal arches as early as E9.5
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• exhibit an increase in apoptosis of neural crest cells migrating from rhombomeres 6-8
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• those that survive to birth die postnatally due to lethal vascular defects in 30% and severe craniofacial defects in 100% of mutants
|
|
• 25% die prior to birth
|
|
• 30% show lethal vascular defects, however outflow tract development is normal
|
|
• 95% have abnormal fourth pharyngeal arch artery formation at E10.5
• migration and early differentiation of the 4th pharyngeal arch artery endothelial cells occurs normally but subsequent vascular organization fails such that at the 35-37 somite stage, endothelial cells remain disorganized and fail to form primitive vascular tubes, long after this vessel is patent and pericyte recruitment is under way in controls
|
|
• 33% display bilateral aplasia of the fourth and sixth pharyngeal arch arteries at E10.5
|
|
• 12% show bilateral hypoplasia of the 4th pharyngeal arch arteries
|
|
• 33% display bilateral aplasia of the fourth and sixth pharyngeal arch arteries at E10.5
|
|
• exhibit an abnormally large third pharyngeal arch artery
|
|
• 30% of E18.5 mutants have interrupted aortic arch type B (IAAB)
|
|
• 13% exhibit circumflex right aortic arch (RAA) or RAA with right ductus arteriosus
|
|
• 46% exhibit coronary artery anomalies, in isolation or associated with other vascular defects
|
|
• subclavian artery anomalies
|
|
• 80% exhibit retroesophageal right subclavian artery or abnormal subclavian branching associated with other defects
|
|
• 100% show severe craniofacial malformations
|
|
• 95% have abnormal fourth pharyngeal arch artery formation at E10.5
• migration and early differentiation of the 4th pharyngeal arch artery endothelial cells occurs normally but subsequent vascular organization fails such that at the 35-37 somite stage, endothelial cells remain disorganized and fail to form primitive vascular tubes, long after this vessel is patent and pericyte recruitment is under way in controls
|
|
• 33% display bilateral aplasia of the fourth and sixth pharyngeal arch arteries at E10.5
|
|
• 12% show bilateral hypoplasia of the 4th pharyngeal arch arteries
|
|
• 33% display bilateral aplasia of the fourth and sixth pharyngeal arch arteries at E10.5
|
|
• exhibit an abnormally large third pharyngeal arch artery
|
|
• exhibit severe pharyngeal arch 1 hypoplasia and hypoplasia and fusion of the more caudal pharyngeal arches as early as E9.5
|
|
• 95% have abnormal fourth pharyngeal arch artery formation at E10.5
• migration and early differentiation of the 4th pharyngeal arch artery endothelial cells occurs normally but subsequent vascular organization fails such that at the 35-37 somite stage, endothelial cells remain disorganized and fail to form primitive vascular tubes, long after this vessel is patent and pericyte recruitment is under way in controls
|
|
• 33% display bilateral aplasia of the fourth and sixth pharyngeal arch arteries at E10.5
|
|
• 12% show bilateral hypoplasia of the 4th pharyngeal arch arteries
|
|
• 33% display bilateral aplasia of the fourth and sixth pharyngeal arch arteries at E10.5
|
|
• exhibit an abnormally large third pharyngeal arch artery
|
|
• exhibit an increase in apoptosis of neural crest cells migrating from rhombomeres 6-8
|
|
• exhibit severe pharyngeal arch 1 hypoplasia and hypoplasia and fusion of the more caudal pharyngeal arches as early as E9.5
|
|
• exhibit an increase in apoptosis of neural crest cells migrating from rhombomeres 6-8
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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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