Phenotypes associated with this allele
|
Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Myocdtm1Msp mutation
(0 available);
any
Myocd mutation
(53 available)
|
|
|
cardiovascular system
|
• neonatal primary cardiomyocytes transduced with an adenovirus expressing cre recombinase (Ad-cre) show loss of the loosely arranged myofibrils within 72 hours of Ad-cre infection
|
|
• cardiomyocytes infected with Ad-cre show widespread apoptosis
|
cellular
|
• cardiomyocytes infected with Ad-cre show widespread apoptosis
|
muscle
|
• neonatal primary cardiomyocytes transduced with an adenovirus expressing cre recombinase (Ad-cre) show loss of the loosely arranged myofibrils within 72 hours of Ad-cre infection
|
|
• cardiomyocytes infected with Ad-cre show widespread apoptosis
|
|
Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
H2az2Tg(Wnt1-cre)11Rth mutation
(2 available);
any
H2az2 mutation
(26 available)
Myocdtm1Msp mutation
(0 available);
any
Myocd mutation
(53 available)
|
|
|
mortality/aging
|
• majority of mutants die before P3
|
cardiovascular system
|
• the architecture of the neointima and tunica media of the ductus arteriosus is disturbed
• increase in fibronectin and laminin in the ductus arteriosus
|
|
• all mutants at P2 exhibit patent ductus arteriosus
• E16.5 mutants exhibit diminished expression of smooth muscle cell contractile proteins in the ductus arteriosus
• however, patterning of the cardiac outflow tract and great arteries is normal
|
|
• the smooth muscle cells of the ductus arteriosus are heterogeneous in size with a loss of spindle-like cell morphology
• the smooth muscle cells of the ductus arteriosus have relatively few myofibers and show an increase in synthetic organelles, including the rough ER and Golgi
|
homeostasis/metabolism
muscle
|
• the smooth muscle cells of the ductus arteriosus are heterogeneous in size with a loss of spindle-like cell morphology
• the smooth muscle cells of the ductus arteriosus have relatively few myofibers and show an increase in synthetic organelles, including the rough ER and Golgi
|
cellular
|
• all mutants at P2 exhibit patent ductus arteriosus
• E16.5 mutants exhibit diminished expression of smooth muscle cell contractile proteins in the ductus arteriosus
• however, patterning of the cardiac outflow tract and great arteries is normal
|
|
Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation
(5 available);
any
A1cf mutation
(39 available)
Myocdtm1Msp mutation
(0 available);
any
Myocd mutation
(53 available)
|
|
|
mortality/aging
|
• 4 month old mice treated with tamoxifen become lethargic within 3-4 days of tamoxifen exposure and die within 7 days
|
cardiovascular system
|
• derangements in cardiomyocyte structure and myofibrillar organization are seen throughout the hearts of tamoxifen-treated adult mice
• myofibrillar striations are absent in tamoxifen-treated hearts
• cardiomyocytes of tamoxifen-treated adult mice exhibit indistinct desmosomes and adherens junctions
|
|
• structure of the intercalated disc is disrupted in the hearts of tamoxifen-treated adult mice
|
|
• loss of cardiomyocytes in tamoxifen-treated adults
|
|
• cardiomyocyte disarray with myocyte loss in hearts of tamoxifen-treated adult mice
• sparse, randomly oriented myofibers are seen throughout the sarcoplasm of hearts of tamoxifen-treated adult mice
|
|
• hearts of tamoxifen-treated adult mice are enlarged
|
|
• hearts of tamoxifen-treated adult mice show large pericardial effusions
|
|
• fibrosis in hearts of tamoxifen-treated adult mice
|
|
• 6 days after tamoxifen treatment, adult mice exhibit severe dilated cardiomyopathy involving all 4 chambers
|
|
• mean ejection fraction is decreased in tamoxifen-treated adult mice
|
|
• widespread cardiomyocyte apoptosis in tamoxifen-treated adult mice
|
growth/size/body
|
• hearts of tamoxifen-treated adult mice are enlarged
|
cellular
|
• widespread cardiomyocyte apoptosis in tamoxifen-treated adult mice
|
homeostasis/metabolism
muscle
|
• derangements in cardiomyocyte structure and myofibrillar organization are seen throughout the hearts of tamoxifen-treated adult mice
• myofibrillar striations are absent in tamoxifen-treated hearts
• cardiomyocytes of tamoxifen-treated adult mice exhibit indistinct desmosomes and adherens junctions
|
|
• structure of the intercalated disc is disrupted in the hearts of tamoxifen-treated adult mice
|
|
• loss of cardiomyocytes in tamoxifen-treated adults
|
|
• cardiomyocyte disarray with myocyte loss in hearts of tamoxifen-treated adult mice
• sparse, randomly oriented myofibers are seen throughout the sarcoplasm of hearts of tamoxifen-treated adult mice
|
|
• 6 days after tamoxifen treatment, adult mice exhibit severe dilated cardiomyopathy involving all 4 chambers
|
|
• mean ejection fraction is decreased in tamoxifen-treated adult mice
|
|
• widespread cardiomyocyte apoptosis in tamoxifen-treated adult mice
|
|
• loss of sarcomeres in the hearts of tamoxifen-treated adult mice
|
|
Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Myocdtm1Msp mutation
(0 available);
any
Myocd mutation
(53 available)
Tg(Pax3-cre)1Joe mutation
(0 available)
|
|
|
mortality/aging
cardiovascular system
|
• all mutants at P2 exhibit patent ductus arteriosus
• E16.5 mutants exhibit diminished expression of smooth muscle cell contractile proteins in the ductus arteriosus
• however, patterning of the cardiac outflow tract and great arteries is normal
|
cellular
|
• all mutants at P2 exhibit patent ductus arteriosus
• E16.5 mutants exhibit diminished expression of smooth muscle cell contractile proteins in the ductus arteriosus
• however, patterning of the cardiac outflow tract and great arteries is normal
|
|
Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Myocdtm1Msp mutation
(0 available);
any
Myocd mutation
(53 available)
Tg(Myh6-cre)2182Mds mutation
(3 available)
|
|
|
mortality/aging
|
• 90% of mice die by 10 months of age and no mice survive beyond 1 year of age
|
|
• about 20% of mice die before 3 weeks of age
|
cardiovascular system
|
• extensive loss of myofibrillar striations
|
|
• intercalated discs of hearts appear abnormal
• serpiginous intercalated discs with indistinct desmosomes and adherens junctions
|
|
• hearts show extensive loss of cardiomyocytes
|
|
• both the left and right atrium are enlarged in 10 month old mice
|
|
• four-chamber enlargement in 10 month old mice
|
|
• both the left and right ventricles are enlarged in 10 month old mice
|
|
• 11.2% of the left ventricle myocardium shows fibrosis compared to 0.46% in controls
|
|
• mice develop lethal dilated cardiomyopathy
|
|
• systolic function is depressed
• mean ejection fraction is reduced (24.5% vs 57.8% in controls)
|
|
• echocardiography shows enlargement of the left atrium, left ventricle, right atrium, and right ventricle in 10 month old hearts
|
homeostasis/metabolism
muscle
|
• extensive loss of myofibrillar striations
|
|
• intercalated discs of hearts appear abnormal
• serpiginous intercalated discs with indistinct desmosomes and adherens junctions
|
|
• hearts show extensive loss of cardiomyocytes
|
|
• mice develop lethal dilated cardiomyopathy
|
|
• systolic function is depressed
• mean ejection fraction is reduced (24.5% vs 57.8% in controls)
|
|
• shortened, hypercontracted sarcomeres in hearts
|
growth/size/body
|
• four-chamber enlargement in 10 month old mice
|