Phenotypes associated with this allele

• Allele Symbol: Sod2^{tm1(tetO-Sod2)Evbo}
• Allele Name: targeted mutation 1, Eva Bober
• Allele ID: MGI:4818481
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Sod2^tm1(tetO-Sod2)Evbo/Sod2^tm1(tetO-Sod2)Evbo	involves: 129S4/SvJae * C57BL/6	MGI:4818490
ht2	Sod2^tm1(tetO-Sod2)Evbo/Sod2^+	involves: 129S4/SvJae * C57BL/6	MGI:4818491

Genotype
MGI:4818490

hm1

• Allelic Composition: Sod2^{tm1(tetO-Sod2)Evbo}/Sod2^{tm1(tetO-Sod2)Evbo}
• Genetic Background: involves: 129S4/SvJae * C57BL/6

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

mortality/aging

postnatal lethality, complete penetrance ( J:162190 )

• mice die 1 to 3 weeks after birth

behavior/neurological

impaired balance ( J:162190 )

decreased locomotor activity ( J:162190 )

cardiovascular system

increased cardiomyocyte apoptosis ( J:162190 )

• in the superficial layers of the left ventricular wall

cellular

increased cardiomyocyte apoptosis ( J:162190 )

• in the superficial layers of the left ventricular wall

oxidative stress ( J:162190 )

• under normoxic conditions, primary fibroblasts exhibit increased production of reactive oxygen species compared with similarly treated wild-type cells

growth/size/body

decreased body size ( J:162190 )

muscle

increased cardiomyocyte apoptosis ( J:162190 )

• in the superficial layers of the left ventricular wall

Genotype
MGI:4818491

ht2

• Allelic Composition: Sod2^{tm1(tetO-Sod2)Evbo}/Sod2⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

cardiovascular system

increased myocardial fiber size ( J:162190 )

myocardium necrosis ( J:162190 )

abnormal heart left ventricle morphology ( J:162190 )

• mice exhibit increased left ventricular internal diameter in systole compared with wild-type mice

cardiac fibrosis ( J:162190 )

decreased ventricle muscle contractility ( J:162190 )

• left ventricular fractional area change, ejection fraction, and fractional shortening are decreased compared to in wild-type mice

increased cardiomyocyte apoptosis ( J:162190 )

• mice are more susceptible to doxorubicin treatment with increased myocardial apoptosis, senescence, and degeneration compared with wild-type mice

homeostasis/metabolism

increased physiological sensitivity to xenobiotic ( J:162190 )

• mice are more susceptible to doxorubicin treatment with increased myocardial apoptosis, senescence, and degeneration compared with wild-type mice

muscle

increased myocardial fiber size ( J:162190 )

myocardium necrosis ( J:162190 )

decreased ventricle muscle contractility ( J:162190 )

• left ventricular fractional area change, ejection fraction, and fractional shortening are decreased compared to in wild-type mice

increased cardiomyocyte apoptosis ( J:162190 )

• mice are more susceptible to doxorubicin treatment with increased myocardial apoptosis, senescence, and degeneration compared with wild-type mice

cellular

myocardium necrosis ( J:162190 )

increased cardiomyocyte apoptosis ( J:162190 )

• mice are more susceptible to doxorubicin treatment with increased myocardial apoptosis, senescence, and degeneration compared with wild-type mice