Phenotypes associated with this allele

• Allele Symbol: Slc25a3^tm1.1Jmol
• Allele Name: targeted mutation 1.1, Jeffery Molkentin
• Allele ID: MGI:6198542
• Summary: 1 genotype

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Slc25a3^tm1.1Jmol/Slc25a3^tm1.1Jmol A1cf^Tg(Myh6-cre/Esr1*)1Jmk/?	involves: 129S6/SvEvTac * C57BL/6 * FVB/N	MGI:6201133

Genotype
MGI:6201133

cn1

• Allelic Composition: Slc25a3^tm1.1Jmol/Slc25a3^tm1.1Jmol; A1cf^{Tg(Myh6-cre/Esr1*)1Jmk}/?
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6 * FVB/N

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

cardiovascular system

abnormal cardiac muscle tissue morphology ( J:229795 )

• 80% increase in cardiomyocyte cross-section 10 weeks after tamoxifen treatment

increased heart weight ( J:229795 )

• heart weight to body weight ratio is increased by 300% 10 weeks after tamoxifen treatment

cardiac hypertrophy ( J:229795 )

• severe cardiac hypertrophy and myopathy, but no fibrosis 10 weeks after tamoxifen treatment

decreased heart left ventricle muscle contractility ( J:229795 )

• reduced fractional shortening with greater left ventricular chamber in diastole 10 weeks after tamoxifen treatment

cardiomyopathy ( J:229795 )

• severe cardiac hypertrophy and myopathy, but no fibrosis 10 weeks after tamoxifen treatment

cellular

abnormal mitochondrial ATP synthesis coupled electron transport ( J:229795 )

• rate of mitochondrial ATP synthesis is decreased by 45% following tamoxifen administration, however, cardiac ventricular performance is not affected and 10 weeks after treatment ATP levels are unchanged

• mitochondrial inorganic phosphate (Pi) uptake is decreased in cardiac mitochondria two weeks after tamoxifen administration

increased mitochondrial fission ( J:229795 )

• mitochondrial hyperproliferation occurs 10 weeks after tamoxifen treatment

homeostasis/metabolism

abnormal calcium ion homeostasis ( J:229795 )

• sarcoplasmic reticulum Ca²⁺ load is increased following tamoxifen administration, however, overall Ca²⁺ reuptake time is not changed

muscle

abnormal cardiac muscle tissue morphology ( J:229795 )

• 80% increase in cardiomyocyte cross-section 10 weeks after tamoxifen treatment

decreased heart left ventricle muscle contractility ( J:229795 )

• reduced fractional shortening with greater left ventricular chamber in diastole 10 weeks after tamoxifen treatment

cardiomyopathy ( J:229795 )

• severe cardiac hypertrophy and myopathy, but no fibrosis 10 weeks after tamoxifen treatment

abnormal sarcomere morphology ( J:229795 )

• sarcomeric disarray with fragmented and disrupted mitochondria 10 weeks after tamoxifen treatment

nervous system

abnormal channel response ( J:229795 )

• swelling of the mitochondrial permeability transition pore (MPTP) as a result of Ca²⁺ overload is reduced as compared to wild-type in cardiac mitochondria following tamoxifen administration

growth/size/body

increased heart weight ( J:229795 )

• heart weight to body weight ratio is increased by 300% 10 weeks after tamoxifen treatment

cardiac hypertrophy ( J:229795 )

• severe cardiac hypertrophy and myopathy, but no fibrosis 10 weeks after tamoxifen treatment