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Phenotypes Associated with This Genotype
Genotype
MGI:5908988
Allelic
Composition
Tg(Myh6-Tnnt2*R92W)1Jcf/0
Genetic
Background
B6.Cg-Tg(Myh6-Tnnt2*R92W)1Jcf
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• adult hearts show myocyte disarray and degeneration, mild inflammatory cell infiltration, occasional hypertrophied cells, and minimal fibrosis
• isolated myofilament lysis and discontinuity in adult ventricular myocytes
• adult hearts show myocyte degeneration
• decrease in myocyte size that results in a decrease in ventricular mass
• hearts are smaller
• heart weigh/body weight ratio is smaller
• ventricular mass is decreased by 14% in 6 month old mice
• 6 month old mice exhibit mild degrees of myofibrillar lysis and prominent atrial natriuretic factor granules in left ventricular tissue
• however, no sarcomere loss or destruction, mitochondrial abnormalities, or apoptotic nuclei are seen in left ventricular tissue
• hearts exhibit impaired systolic performance at baseline and with inotropic challenge
• diastolic function, as indicated by increases in end-diastolic pressure and decreases in the rate of relaxation, is impaired, with hearts unable to increase their rate of relaxation in response to increased perfusate of calcium
• hearts are less able to increase developed pressure upon inotropic challenge
• left ventricular systolic pressure and the rate of pressure development (+dP/dt) are lower in response to increasing calcium concentrations
• hearts exhibit a more severe cardiomyopathy than Tg(Myh6-Tnnt2*R92L)1Jcf /0 mice
• maker analysis shows early activation of the fetal gene or hypertrophic gene program indicating early disease onset, however, overt ventricular hypertrophy is not seen

muscle
• isolated myofilament lysis and discontinuity in adult ventricular myocytes
• adult hearts show myocyte degeneration
• decrease in myocyte size that results in a decrease in ventricular mass
• hearts exhibit impaired systolic performance at baseline and with inotropic challenge
• diastolic function, as indicated by increases in end-diastolic pressure and decreases in the rate of relaxation, is impaired, with hearts unable to increase their rate of relaxation in response to increased perfusate of calcium
• hearts exhibit a more severe cardiomyopathy than Tg(Myh6-Tnnt2*R92L)1Jcf /0 mice
• maker analysis shows early activation of the fetal gene or hypertrophic gene program indicating early disease onset, however, overt ventricular hypertrophy is not seen
• adult ventricular myocytes exhibit dilated sarcomeric reticulum

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
hypertrophic cardiomyopathy 2 DOID:0110308 OMIM:115195
J:104369


Contributing Projects:
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
06/04/2019
MGI 6.14
The Jackson Laboratory