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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Trim55tm1Cpat
targeted mutation 1, Cam Patterson
MGI:3785406
Summary 4 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Trim55tm1Cpat/Trim55tm1Cpat involves: 129 * C57BL/6 MGI:3785745
cx2
Trim55tm1Cpat/Trim55tm1Cpat
Trim63tm1Glas/Trim63tm1Glas
involves: 129S1/Sv * C57BL/6 MGI:6258325
cx3
Trim55tm1Cpat/Trim55tm1Cpat
Trim63tm1Glas/Trim63+
involves: 129S1/Sv * C57BL/6 MGI:6258326
cx4
Trim55tm1Cpat/Trim55+
Trim63tm1Glas/Trim63tm1Glas
involves: 129S1/Sv * C57BL/6 MGI:6258327


Genotype
MGI:3785745
hm1
Allelic
Composition
Trim55tm1Cpat/Trim55tm1Cpat
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trim55tm1Cpat mutation (0 available); any Trim55 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
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




Genotype
MGI:6258325
cx2
Allelic
Composition
Trim55tm1Cpat/Trim55tm1Cpat
Trim63tm1Glas/Trim63tm1Glas
Genetic
Background
involves: 129S1/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trim55tm1Cpat mutation (0 available); any Trim55 mutation (33 available)
Trim63tm1Glas mutation (0 available); any Trim63 mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 4 of 11 mice that survive to adulthood die between 0.7 to 3.3 months of age
• 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
• significant decrease in the expected number of pups of born, with approximately 67.1% of mutants dying in utero

growth/size/body
• 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

cardiovascular system
• hearts of mice that die on average at P14 show gross mitochondria abnormalities
• 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
• 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
• 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
• 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
• 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

homeostasis/metabolism
• mice that die within the first 2 weeks of life exhibit edematous lungs

muscle
• hearts of mice that die on average at P14 show gross mitochondria abnormalities
• 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
• 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
• hearts of mice that die on average at P14 show M line defects
• hearts of mice that die on average at P14 show Z disc defects

respiratory system
• mice that die within the first 2 weeks of life exhibit edematous lungs




Genotype
MGI:6258326
cx3
Allelic
Composition
Trim55tm1Cpat/Trim55tm1Cpat
Trim63tm1Glas/Trim63+
Genetic
Background
involves: 129S1/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trim55tm1Cpat mutation (0 available); any Trim55 mutation (33 available)
Trim63tm1Glas mutation (0 available); any Trim63 mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• mice exhibit a normal cardiac phenotype and no deficit in fractional shortening




Genotype
MGI:6258327
cx4
Allelic
Composition
Trim55tm1Cpat/Trim55+
Trim63tm1Glas/Trim63tm1Glas
Genetic
Background
involves: 129S1/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trim55tm1Cpat mutation (0 available); any Trim55 mutation (33 available)
Trim63tm1Glas mutation (0 available); any Trim63 mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• mice exhibit a normal cardiac phenotype and no deficit in fractional shortening





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last database update
05/07/2024
MGI 6.23
The Jackson Laboratory