Analysis Tools|
Allele Symbol Allele Name Allele ID |
Myod1tm1Jae targeted mutation 1, Rudolf Jaenisch MGI:1857221 |
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| Summary |
15 genotypes
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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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• skeletal myogenesis is not suppressed by genotoxins unlike in wild-type mice
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• skeletal myogenesis is not suppressed by genotoxins unlike in wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• more so than in Pax7tm1.1Thbr/Pax7tm1.1Thbr Myf5tm1(cre)Mrc/Myf5+ mice at day 110
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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 |
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• double homozygous mutants display postnatal lethality
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• no skeletal myogenesis is seen at any developmental stage
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• mutants lack skeletal muscle throughout the body including the head
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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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• die within minutes of birth
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• E18.5 mutants show a reduction in body mass
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• marker analysis indicates that myoblasts are present in normal muscles but they are unable to differentiate into muscle fibers
marker analysis indicates that myoblasts are present in normal muscles but they are unable to differentiate into muscle fibers
• myoblasts from neonates are unable to differentiate in vitro
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• severe muscle deficiency with almost no muscle fibers; the few fibers that are present are extremely thin and underdeveloped
• tongue, back, limb, and skeletal muscle are all affected comparably unlike in single Myog homozygous mutants
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• the average lengths of the ossified portions of the ribs are 30% shorter than normal at E15.5, however the ribs reach the sternum
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• myogenesis is arrested at the level seen in single homozygous Myog mutants
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mutants are normal, viable and fertile and appear to have normal muscle
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• die within minutes after birth due to an inability to breathe
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• decrease in body mass at E16.5
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• nuclei are centrally located instead of in the periphery as in wild-type
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• severe skeletal muscle deficiency with only residual muscle fibers surrounded by mononucleated cells
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• appear to lack skeletal muscle beginning at E14.5
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• show rib defects indistinguishable from Myf6tm1Eno homozygotes
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• accumulate brown fat at the apex of the neck beginning at E14.5
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• die within minutes after birth due to an inability to breathe
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Dmdmdx/? Myod1tm1Jae/Myod1tm1Jae mice develop cardiomyopathy
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• premature death around 12 months of age
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• ventricles contain regions in which individual cardiac myocytes are enlarged; these hypertrophic myocytes are more common in the left ventricle than the right ventricle
• cardiac myocyte hypertrophy precedes necrosis
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• fibrotic areas are composed of necrotic myocytes
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• hearts show an increase in ventricular diameter without a change in the thickness of the ventricular wall
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• more than 50% of mutants show evidence of fibrosis at 10 months of age, while more than 80% display extensive fibrosis by 12 months of age
• fibrosis is seen in the left ventricle and only rarely in the right ventricle and are confined primarily to the epicardial region of the left ventricle
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• fibrotic areas are composed of necrotic myocytes associated with interstitial fibrosis
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• progressive development of dilated cardiomyopathy that is evident by 5 months of age
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• ventricles contain regions in which individual cardiac myocytes are enlarged; these hypertrophic myocytes are more common in the left ventricle than the right ventricle
• cardiac myocyte hypertrophy precedes necrosis
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• fibrotic areas are composed of necrotic myocytes
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• progressive development of dilated cardiomyopathy that is evident by 5 months of age
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• fibrotic areas are composed of necrotic myocytes associated with interstitial fibrosis
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| Duchenne muscular dystrophy | DOID:11723 |
OMIM:310200 |
J:52248 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mutant embryos do not form skeletal myotubes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• only the double homozygous mutants display postnatal lethality
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• skeletal muscle differentiation is seen at E12.5 however myogenesis is still severely impaired such that mutants essentially lack skeletal muscle at birth
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• mutants essentially lack skeletal muscle throughout the body including the head
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• only the double homozygous mutants display postnatal lethality
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• skeletal muscle differentiation is seen at E12.5 however myogenesis is still severely impaired such that mutants essentially lack skeletal muscle at birth
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• mutants essentially lack skeletal muscle throughout the body including the head
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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 12/17/2024 MGI 6.24 |
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