Analysis Tools|
Allele Symbol Allele Name Allele ID |
Trim55tm1Cpat targeted mutation 1, Cam Patterson MGI:3785406 |
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| Summary |
4 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• despite a predicted role in titin dynamics, no structural or functional abnormalities are seen in the heart and hypertrophic responses to transaortic constriction are similar to those in wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 4 of 11 mice that survive to adulthood die between 0.7 to 3.3 months of age
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• of the mice that are born alive, 19 of 25 die between birth and P23, with an average death at P14, while the remaining 6 survive to adulthood
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• significant decrease in the expected number of pups of born, with approximately 67.1% of mutants dying in utero
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• mice that die in utero show extensive cardiac hypertrophy, with the majority of thoracic cavity taken up by the enlarged heart
• mice surviving birth develop cardiac hypertrophy showing increased heart weight/tibia length, increased gross histological size, and increased cardiomyocyte cross sectional area
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• hearts of mice that die on average at P14 show gross mitochondria abnormalities
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• mice that die in utero show extensive cardiac hypertrophy, with the majority of thoracic cavity taken up by the enlarged heart
• mice surviving birth develop cardiac hypertrophy showing increased heart weight/tibia length, increased gross histological size, and increased cardiomyocyte cross sectional area
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• mice that die in utero show presence of cardiac fibrosis
• mice that die within the first several weeks of life show widespread cardiac fibrosis
• however, mice that survive to adulthood do not exhibit cardiac fibrosis
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• mice that survive to adulthood show defects in cardiac function, including decreased fractional shortening and ejection fraction at 6 weeks of age, and a dramatic decrease in the percentage of fractional shortening at 12 weeks of age
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• echocardiography at 12 weeks of age shows increased left ventricular mass index and mass, increased interventricular septal thickness in systole, increased posterior wall thickness in diastole, decreased posterior wall thickness in systole, increased left ventricular end-diastolic dimension and left ventricular end-systolic dimension and reduced percent ejection fraction
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• cause of death in mice that die in the first 2 weeks of life appears to be heart failure, as indicated by a decrease in cardiac function and edematous lungs
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• mice that die within the first 2 weeks of life exhibit edematous lungs
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• hearts of mice that die on average at P14 show gross mitochondria abnormalities
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• mice that survive to adulthood show defects in cardiac function, including decreased fractional shortening and ejection fraction at 6 weeks of age, and a dramatic decrease in the percentage of fractional shortening at 12 weeks of age
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• hearts from mice that die on average at P14 exhibit disrupted sarcomeres, with both Z disc and M line defects
• however, no sarcomere defects are seen in skeletal muscle
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• hearts of mice that die on average at P14 show M line defects
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• hearts of mice that die on average at P14 show Z disc defects
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• mice that die within the first 2 weeks of life exhibit edematous lungs
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice exhibit a normal cardiac phenotype and no deficit in fractional shortening
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice exhibit a normal cardiac phenotype and no deficit in fractional shortening
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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 12/10/2024 MGI 6.24 |
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